I.
BACKGROUND AND TERMINOLOGIES
A. PARASITES – organisms that live on and obtain
their nutrients from another organism
B. PARASAITOLOGY – study of parasites
C. INFECTION - parasites invading in the body
D. INFESTATION – invading on the body
E. DISEASE - process with characteristic symptoms,
emerged, determining an effective means of
healing infected people
F. VECTORS – transport carriers
G. MODE OF TRANSMISSION - the means whereby
a parasite enters an unsuspecting host
IV.
II.
PARASITE-HOST RELATIONSHIPS
- MAIN FOCUS OF THIS RESEARCH:
1. Recognition of these relationships
2. Search for patterns
3. Development of methodologies to study these
patterns
SEE TABLE 1-1
III.
PARASITIC LIFE CYCLES
- 3 MAIN COMPONENTS:
1. Mode of transmission
2. Infective stage
3. Diagnostic stage
- 2 COMMON PHASES:
1. Route a parasite follows when in or on the
human body
2. Route a parasite follows independently of the
human body
V.
DISEASE PROCESSES AND SYMPTOMS
- MAJOR AREAS AFFECTED:
1. GI and urogenital tracts
2. Blood and tissue
3. Liver, lung, and other major organs
4. Miscellaneous locations (e.g. eye, skin, etc.)
- SYMPTOMS ASSOCIATED WITH PARASITIC
DISEASE PROCESSES
1. Diarrhea
2. Fever
3. Chills
4. Abdominal pain and cramping
5. Elephantiasis (accumulation of lymph)
6. Anemia
7. Vitamin deficiency
8. Bowel obstruction
9. Edema
10. Enlargement of major organs
11. Skin lesions
12. Blindness
TREATMENT
- PARASITE TREATMENT OPTIONS
a. Antiparasitic medications
b. Change in diet
c. Vitamin supplements
d. Fluid replacement
e. Blood transfusion
f. Bed rest
VI.
VII.
VIII.
PREVENTION AND CONTROL
- Designed to break the transmission cycle are
crucial for successful parasite eradication
- Some strategies:
a. Development and implementation of parasite
awareness education programs
b. Use of insecticides and other chemicals
c. Use of protective clothing
d. Use of protective netting
e. Proper water treatment
f. Good personal hygiene
g. Proper sanitation practices
h. Proper handling, cooking, and protection of
food
i. Avoidance of unprotected sexual relations
SPECIMEN PROCESSING AND LABORATORY
DIAGNOSIS
1. O&A – aka ova (eggs) and parasites
2. Giesma stain – blood (sample for parasite study)
3. Cellophane tape preparation – pinworm eggs
4. Enterotest (string test) – recovery of several
parasites
PARASITE NOMENCLATURE AND
CLASSIFICATION
1. Written in italics
2. Genus + species
3. Variations of genus names are used to denote
the disease associated with the parasite
4. When first appeared in documents, the whole
name is written out
5. -iasis → denotes diseases/conditions
-
3 MAJOR GROUPS OF CLINICALLY
SIGNIFICANT PARASITES:
1. Single-celled parasites (protozoa)
2. Multicellular worms (metazoan helminths
3. Arthropods (animalia)
Specimen Collection and
Processing
•
•
•
•
•
Collection and Transportation
Fixatives for Preservation
Processing
Stool Screening Methods
Other Specimens and laboratory
techniques
COLLECTION AND TRANSPORT
• Protozoan forms (trophozoites and
cysts) and helminth stages (egg,
larvae, proglottids, and adult
worms) are found in stool samples.
• Typical stool collection protocol:
o 3 specimens in 10 days
• Amebiasis
o 6 specimens in 14 days
SAMPLE LABELLING:
• Patient’s name
• Identification number
• Physician’s name
• Date and time of collection
• Age
• Gender
➢ Trophozoite motility – fresh
sample is required.
➢ Protozoan cysts helminth egg and
larvae are not sensitive.
➢ Liquid samples: Processed within
30 mins. (Presence of
trophozoites)
➢ Semi-formed stool samples:
Evaluated within 1 hour (Presence
of trophozoites and cysts)
➢ Formed samples: Can be held
within 24 hours.
➢ Guidelines are not met; the
samples must be preserved.
FIXATIVE AS PRESERVATION:
• Ideal Sample: Freshly collected
stool sample
• Substances that preserve the
morphology of protozoans and
prevent development of helminth
eggs and larvae.
• Ratio is 3:1 (3 parts fixative; 1 part
of stool)
1. Fomalin
2. Polyvinyl Alcohol (PVA)
3. Sodium Acetate Formalin (SAF)
4. Modified Polyvinyl Alcohol
5. Alternative Single Vial Systems
1. FORMALIN
• All-purpose fixative for helminths
and protozoans.
• 2 concentrations:
o 5% - protozoan cysts
o 10% - helminth eggs and
larvae.
• Used for routine direct
examinations and concentration
techniques but NOT for permanent
smears.
ADVANTAGES:
• Easy to prepare
• Preserves specimen up to several
years.
• Long shelf-life
DISADVANTAGES:
• Does not preserve parasite
morphology adequately for
permanent smears.
• Trophozoites may not be
recovered.
• Morphology of cysts and eggs may
fade with time.
• Potential health hazard.
2. POLYVINYL ALCOHOL (PVA)
• Combined with Schaudinn solution
(Zinc Sulfate, Copper Sulfate or
Mercuric Chloride).
ADVANTAGES:
• Choice of permanent stain (Iron
Hematoxylin)
4. MODIFIED POLYVINYL ALCOHOL
(PVA)
• Alternative fixative to Mercurybased PVA by using Copper Sulfate
and Zinc Sulfate.
• Long shelf-life when stored at
room temperature.
• Can be used for concentration
methods and permanent smears.
• Concentration techniques can be
performed (Two-vial system).
• Do not provide the same quality of
preservation of protozoan
morphology.
• Trophozoites and cysts of
protozoans, most helminth eggs
can be detected.
• Can be used for preparation in a
permanent stained smear.
DISAVANTAGES:
• Potential health problems
(Mercury in Schaudinn solution).
3. SODIUM ACETATE FORMALIN
(SAF)
• Alternative fixative to PVA and
Schaudinn fixative.
• Used in concentration techniques
and permanent stained smears.
ADVANTAGES:
• Easy to prepare.
• Long-shelf life
• Use for preparing smears for
staining with modified acid-fast
stain for Coccidian cysts.
DISADVANTAGES:
• Addition of Albumin is necessary.
• Protozoan morphology is not clear
in permanent smears.
5. ALTERNATIVE SINGLE-VIAL
SYSTEM
• Single vial systems are free of
Formalin and Mercury.
• Used for concentration techniques
and permanent smears.
• Used in fecal immunoassays.
• Disadvantage:
1. Do not provide the same
quality as Mercury-based
fixative.
2. Organism identification will
be more difficult.
PROCESSING
MACROSCOPIC
- Consistency (degree of moisture)
- Color (Normal: brown)
- Gross abnormalities (adult worms,
proglottids, pus and mucus)
MICROSCOPIC
- Direct methods
- Concentration techniques
- Permanently stained smears
MICROSCOPIC EXAMINATION:
1. Direct Wet Preparation
2. Concentration methods
3. Permanent Stained slides
• DIRECT WET PREPARATION
• “Direct Wet Mount”
• Slide made by mixing a small
portion of unfixed stool with saline
or Iodine.
• To detect the presence of motile
protozoan trophozoites (fresh
samples).
• Direct Saline Wet Preparation
• Direct Iodine Wet Preparation
• Debris sinks at the bottom of the
tube.
• Parasites are lighter thus rises on
the top of the tube.
• Zinc sulfate (1.18-1.20) is used as
the concentrating solution.
ADVANATAGES:
• More fecal debris is removed.
• Cleaner preparation, easier for
microscopic examination.
• CONCENTRATION
TECHNIQUES:
FORMALIN-ETHYL ACETATE
SEDIMENTATION
- Principle: Specific gravity
- Ethyl Acetate is added to a salinewashed formalin-fixed sample.
- Parasites heavier than the solution
settles in the sediment of the tube.
- Fecal debris are lighter and rises to
the upper layer of the tube.
ADVANTAGES:
• Easy to prepare
• Good recovery of parasites
DISADVANTAGES:
• More fecal debris
• Challenging to microscopist.
ZINC SULFATE FLOTATION
• Principle: Specific gravity
DISADVATAGE:
• Some helminths are dense and will
not float.
• PERMANENT STAINS
• Final procedure in O&P
examination.
• Microscope slides that contains a
fixed sample that has been allowed
to dry and stained.
• Critical portion of the O&P
examination.
• Sample of choice is PVA-prepared
sample. SAF samples can be used
but the stain must be Iron
Hematoxylin.
• Slides can be prepared from fresh
samples but must not be allowed
to dry and place immediately into
a fixative.
• Two common stains:
o WHEATLY TRICHROME
o IRON HEMATOXYLIN
WHEATLY TRICHROME
• Most widely used permanent stain.
• Long shelf life and easy to perform.
• Distinct color differenced between
the cytoplasmic and nuclear
structures.
IRON HEMATOXYLIN
• Excellent morphology of intestinal
protozoa.
• Nuclear detail are stained clearer
and sharper.
SPECIALIZED STAINS
• Modified acid-fast stain
(Cryptosporidum, Isospora,
Cyclospora spp.)
• Do not detect oocysts and spores
of (Coccidian/Sporidia)
• Modified Iron Hematoxylin
(incorporates with Carbolfuchsin
to detect acid-fast parasites;
combined with SAF-preserved
fecal samples.)
STOOL SCREENING METHODS
• “Rapid methods” (obtained as kits
that contain monoclonal antibody).
• Commercial antibody is used to
detect antigens in patient’s
samples.
• Enzyme Immunoassay, DFA &
Membrane Flow Cartridge
Technique.
• E. histolytica, G. intestinalis &
Cryptosporidum spp.
• Highly sensitive and specific but
detects one pathogen at a time.
PART II
• Duodenal material
• Sigmoidoscopy material
• Cellophane type preparation
DUONENAL MATERIAL
• Collected by nasogastric intubation
or by Enteric capsule test
(Enterotest).
• G. intestinalis troph,
Cryptosporidum spp., Isospora
belli, Strongloides stercoralis and
Clonorchis sinensis/ Fasciola
hepatica.
• Examined by wet prep but if >2mL
it can be centrifuged, and
sediments examined.
• Mixed with PVA fixative and
stained using Trichome, Iron
Hematoxylin and/or Modified Acidfast.
• Antigen test: G. intestinalis &
Cryptosporidum spp.,
CELLOPHANE TAPE
• Detection of Enterobius
vermicularis & Taenia spp.
• Specimen is collected in the
morning.
• Proper hygiene, PPEs during
specimen collection to avoid
spreading of the infection.
SIGMOIDOSCOPY MATERIAL
• Colon
• Detecting Entamoeba histolytica
and Coccidian spp.
• Materials from ulcers obtained by
scrapings or aspirations must be
examined by wet preparation and
permanent stains.
OTHER SPECIMENS AND LABORATORY
TECHNIQUES
BLOOD
• Leishmania donovani &
Trypanosoma cruzi, Plasmodium
spp., Babesia spp.
• Trypanosoma cruzi & Mircofilariae
can be detected by observing the
motility in a wet preparation of a
fresh blood sample.
• Can be processed by:
- Knott technique
• Blood smears are prepared from
fresh whole blood without the
anticoagulant (fingertip/ earlobe)/
venipuncture collection with
anticoagulant.
- Buffy coat slides
- Cultures
COLLECTION AND HANDLING
• Blood collection is by aseptic
technique.
• Site for puncture: Earlobe /
fingertip
• Capillary blood must be freeflowing, not contaminated with
alcohol.
• Anticoagulants can cause
distortion to staining thus affecting
the morphology.
• Blood specimens are collected in
EDTA tubes.
• MALARIA – smears are prepared
within 1hour.
• Timing of obtaining blood samples
varies.
THICK SMEARS:
•
•
•
•
PROCESSING:
Satisfactory for SCREENING.
Dehemoglobinized (more conc.)
Few in number / thin smears (-)
Inreased in detection of malarial
parasites
• RBCs lysed (poor morphology)
• Blood sample processing:
THIN SMEARS:
- Preparing thick and thin
smears
- Staining using permanent
smears
- Microscopic examination
• BEST VIEW of Malarial parasites in
RBCs
• Recommended for species
identification
5. Stain the sediment with
Giemsa.
PERMANENT STAINS:
WRIGHT’S STAIN:
• Contains the fixative and stain in
one solution.
• Yields satisfactory results
GIEMSA STAIN:
• The fixative and stain are separate.
• Preferred stain because it allows
detection of parasite detail
necessary for species
identification.
KNOTT TECHNIQUE:
• Designed to concentrate blood
samples suspected with
Microfilariae.
• Procedure:
1. Combine 1mL of blood with
10mL of 2% Formalin in a
centrifuge tube.
2. Mixture will thoroughly
mixed.
3. Spun for 1 min. at 500 x g.
4. Thick slides are made and
dried.
BUFFY COAT SLIDES:
• Layer of WBCs between plasma
and RBCs (centrifuged).
• Extracted from blood specimens
and stained with Giemsa
(Leishmania & Trypanosoma).
• Procedure:
1. Collected oxalated/ citrated
blood and place it in a
Wintrobe tube.
2. Spin for 30 mins at 100xg
(tubes are capped tightly).
3. Centrifugation produces 3
layers: Packed RBCs, buffy
coat and plasma.
4. Extract the buffy coat using
a capillary pipette.
CULTURES:
• Blood culture as well as bone
marrow and tissue.
• Favorable results for the recovery
of Leishmania spp. & Trypanosoma
cruzi.
• It uses Novy-MacNeal-Nicolle
(NNN) medium.
• Negative cultures are held for 1
month.
• Procedure:
• NNN slant is inoculated by adding
a drop of blood/ tissue.
• Penicillin is added.
• Periodic examination under 400x
CEREBROSPINAL FLUID
• Diagnosis of Amebic conditions
(African Sleeping Sickness)
• Wet preparation (Naegleria fowleri
& Acanthamoeba spp.,
Trypanosoma spp.)
• Giemsa, Trichrome and Modified
Trichrome stain is used.
• If Naegleria & Acanthamoeba spp.
are suspected:
- Cultured on Non-Nutrient
Agar seeded with E. coli.
- CSF sediment is inoculated,
sealed and incubated at 35
- Examine plate, the amoeba
feeding on the the bacteria.
• Other parasites: Toxoplasma
gondii, Microsporidia, Taenia
solium cysticerus larvae and
Echinococcus spp.
OTHER STERILE FLUIDS:
• Cystic fluid
• Aspirates
• Peritoneal fluid
• Pleural fluid
• Bronchial washings
TISSUE AND BIOPSY SEPCIMEN
• Recovery of intracellular parasites:
Leishmania spp. & Toxoplasma
gondii.
• Free-living amoeba, Trypanosoma
spp., Trichinella spiralis &
Microsporidia
• Hepatic abscess: E. histolytica
SPUTUM:
• Collected and tested from patients
suspected with Lung fluke:
Paragonimus westermanii
• Hyperinfection by Strongyloides
stercoralis
• Other parasitic infections:
Microsporidia, E. histolytica, E.
gingivalis, A. lumbricoides and
hookworms.
• Early-morning specimen is best
and should be collected in a
mouth-wide container with screwcap lid.
• Saliva must not be mixed with the
sputum.
• Examined directly by wet preps/
conc. N-acetylcysteine.
URINE AND GENITAL SECRETIONS:
• Urine – specimen of choice for
Schistosoma haematobium &
Trichomonas vaginalis
• Vaginal, urethral and prostatic
excretions are examined for T.
vaginalis
• Specimens are collected on a
swab/ collection cup.
• Saline wet preparation is the
method of choice.
• Latex Agglutination and EIA – T.
vaginalis
• Culture methods: Diagnosis of
STDs
EYE SPECIMENS:
• Corneal scrapings: Acanthamoeba
keratitis
• Other parasites: T. gondii, Loaloa,
Microsporidia
• Collection:
1. Scraping are collected in
airtight container.
2. Kept moist with Saline
solution.
3. Other specimens: Contact
lens/ contact lens solution
4. Can be cultured in an agar
plate with gram-negative
bacteria.
5. Scrapings can be transferred
into glass slides, stained
using Calcofluor white and
examined under Fluorescent
microscopy. (Acanthamoeba
cysts stain apple green)
6. Scrapings can be processed
using histologic methods.
MOUTH SCRAPING AND NASAL
DISCHARGE:
• Mouth scaping is the specimen of
choice for E. gingivalis and T.
tenax.
• Nasal discharged is the specimen
of choice for Naegleria fowleri.
• Both samples are placed in a clean,
airtight container (swab/cup)
1. Obtain skin fluid without
bleeding.
2. Material obtained is placed
on 0.2mL of Saline.
3. Incubate for 30 mins.
4. Read microscopically,
observe the jerky movement
of the microfilariae.
• Can be both prepared using wet
preps and permanent stains.
CULTURE METHODS:
• Not a common means of detecting
parasites.
SKIN SNIPS:
• Useful in detection of Onchocerca
volvulus.
• Procedure:
• Special laboratories and research
facilities may offer these services.
• Parasites that can be cultured:
- Entamoeba histolytica
- Trichomonas vaginalis
- Leishmania spp.
- Trypanosoma cruzi
- Toxoplasma gondii
ANIMAL INOCULATION AND
XENODIAGNOSIS:
• Appropriate specimens from
patients suspected with
Leishmaniasis, Trypanosomiasis
and Toxoplasmosis may be tested
using animal inoculation.
• Mice, guinea pigs and hamsters
are used.
IMMUNOLOGIC TESTING:
• Methods of antigen and antibody
detection.
• Antigen detection methods are
more reliable and positive result is
indicative of current infection.
• Positive antibody tests are
indicative of past infection.
• Not usually offered in routine
laboratories and specimens might
be sent out in reference
laboratories.
• Nucleic acid tests are developed.
• Specimens: blood, lymph nodes,
CSF and bone marrow.
• Only commercial molecular test
available is for T. vaginalis.
• Collected using aseptic technique.
RESULT AND QUALITY CONTROL:
• Post-analytic phase of the
laboratory testing.
• Xenodiagnosis – used for Chagas’
disease.
- Uninfected reduviid bug can
take a blood meal from a
patient, the bug’s feces is
examined to observe the
presence of T. cruzi.
- Used in South America and
Mexico.
• Positive specimen:
- State the scientific name
(genus and species) ex.
Entamoeba histolytica
- Include the stage: cysts,
trophozoites, larvae, eggs
and adults
- Report cells: Presence of
WBCs (semiquantitatively:
rare, few, moderate, many)
• Results of O&P:
- Include a comment regarding the limit
of the test procedures.
• Fecal Immunoassay:
- Indicate the specific parasite that test
for the assay.
- Schistosoma spp.
- Plasmodium spp.
- Babesia spp.
• Charcot-Leyden crystals are also
reported and quantitated when
seen.
QUALITY ASSURANCE:
• Consistent with Microbiology
laboratory.
- Procedure manuals are up
to date and readily available.
- Reagents and solutions must
be labeled, controls in
concentration.
- Stains, centrifuges,
micrometers must be
calibrated.
- Refrigerator and incubator
temperatures must be
recorded.
• Quantitation of parasites is not
indicated.
• Quantitation is important when
these parasites are observed:
- Blastocystis hominis
- Trichuris trichiura
- Clonorchis sinensis
- References for laboratory
training.
- Must also include texts,
atlases, digital images,
reference samples
- Participate in External
quality and internal
proficiency programs
WATER SAMPLES:
• Detection of Cryptosporidium sp.
and Giardia sp. in bulk water
samples.
• FLA (Free-Living Amoeba)
• Cryptosporidium sp. or Giardia sp.
is seeded on NNA with E. coli.
MOLECULAR TESTING:
1. DNA Extraction
2. Polymerase Chain Reaction (PCR)
3. Agarose Gel Electrophoresis
SOIL SAMPLES:
• Rich reservoir for protozoans and
helminths.
• Popular choice for detection of
infective stages of hookworms
(filariform larvae).
• Collected through and Auger (soil
tube).
DNA EXTRACTION:
• Extracting the DNA in the nucleus
of the target organism.
STEP 2: PRECIPITATION
• Commercial kits: QIAGEN,
Mcherey Nagel
• Achieved by:
• FLA: Simple extraction (application
of heat).
• Toxoplasma sp. – additional
method such as freeze-thaw
cycles.
• Helminths – Sonification/ freezethaw cycle.
• Separate the DNA from cellular
debris.
✓ Addition of Na+ ions (makes
the DNA more stable and
less water soluble).
✓ Alcohol (Ethanol/
Isopropanol) – causes the
DNA precipitate out of the
solution since it is alcohol
insoluble.
STEP 3: PURIFICATION
• Rinsing the precipitated DNA with
alcohol to remove unwanted
cellular debris.
• DNA is dissolved in aqueous
solution (ultrapure water).
STEP 1: LYSIS
• Destruction of the cellular and
nuclear wall to liberate DNA.
• Achieved by:
✓ Lysis through detergents or
enzymes (Proteinase K).
✓ Mechanical means by
homogenizer, mortar and
pestle.
•
Tissue sections – cutting into
smaller pieces
2. POLYMERASE CHAIN REACTION
(PCR):
• Most frequently used technique.
• Achieved by using Thermal cycler.
• Purpose: Multiply several copies of
the target gene by priming
complementary sequences.
STEP 1: INTIAL DENTURATION
• Double-helix strands of the target
DNA are uncoiled and separated.
• Temperature: 90 to 95.
STEP 2: ANNEALING
• Also known as Hybridization
• Primers bind to their
complementary bases on each single
strand of DNA.
• Primer sets will bind in the
beginning and end of the chosen
target gene.
• Temperature: 55
- DNA is negatively charged
and will travel to the
positive region when electric
current is applied.
- Migration speed depends on
its molecular weight.
• Comparison:
- DNA ladder is loaded into
the first well.
• Done at 75
- Ethidium Bromide or nontoxic gel dye is added
(better visualization).
• Polymerase read the template
strands and matches the
nucleotides.
- Buffers used are AGE Preps
(Tris-Acetic acid-EDTA
buffers).
STEP 3: POLYMERIZATION
• Results to formation of two helical
strands.
✓ One from the original
strand.
✓ One from the
complementary strand.
• Repeated 30 to 40 times.
3. AGAROSE GEL ELCTROPHOROSIS
• Principle:
- Charged particles is made to
travel in a gel medium
submerged in a buffer
solution.
1.1 MORPHOLOGY AND LIFE CYCLE NOTES
- Equipped with the ability to extend their cytoplasm
in the form of pseudopods (false feet)
- 2 MORPHOLOGIC FORMS IN THE AMEBIC LIFE
CYCLE:
1. TROPHOZOITES - form that feeds, multiplies,
and possesses pseudopods
- Delicate and fragile
- Motile (can produce and use pseudopods)
- Easily destroyed by the gastric juices of
the stomach
- Not usually transmitted to humans
- EXCYSTATION – cyst to trophozoite
(occurring in the ileocecal area of the
intestine)
- ENCYSTATION – trophozoites to cysts;
triggered by a) ameba overpopulation, b)
pH change, c) food supply, d) available
oxygen
2. CYSTS – nonfeeding stage characterized by a
thick protective cell wall designed to protect the
parasite from the harsh outside environment
1.2 LABORATORY DIAGNOSIS
- Trophozoites → soft, liquid, or loose consistency
stools
- Cysts → formed stools
- SALINE WET PREPARATIONS – show motility of
the amebic trophozoites
- IODINE WET PREPARATIONS – better seen
internal cytoplasmic and nuclear structures
- Permanent smear procedures of sample suspected
of having amoebas must be performed to confirm
parasite identification
1.3 PATHOGENESIS AND CLINICAL SYMPTOMS
- A number of patients infected with intestinal
amoebas are asymptomatic.
- In the United States, amebiasis is often found in
immigrants from and people who have traveled to
underdeveloped countries.
1.4 CLASSIFICATION OF THE AMEBAS
- Separated into two categories:
1. Intestinal
2. Extraintestinal – parasites that migrate and/or
take up residence outside the intestines
A. Entamoeba histolytica (intestinal)
B. Entamoeba hartmanni (intestinal)
C. Entamoeba coli (intestinal)
D. Entamoeba polecki (intestinal)
E. Entamoeba nana (intestinal)
F. Iodamoeba butschlii (intestinal)
G. Entamoeba gingivalis (extraintestinal)
H. Naegleria fowleri (extraintestinal)
I. Acanthamoeba species (extraintestinal)
AMOEBA
Entamoeba
histolytica
MORPHOLOGY
LABORATORY
DIAGNOSIS
Antigen tests
Enzyme-linked
immunosorbent assay
(ELISA)
Indirect hemagglutination
(IHA)
Gel diffusion precipitin
(GDP)
Indirect
immunofluorescence
(IIF)
Serologic tests (helpful in
cases of extraintestinal
infections)
LIFE CYCLE NOTES
EPIDEMIOLOGY
CLINICAL SYMPTOMS
Excystation occurs in
the small intestine.
Nuclear division →
cyst producing 8
motile trophozoites
→ settles in lumen of
colon → binary
fission → feeding on
living host cells
Affects 10% of
world’s population
ASYMPTOMATIC CARRIER
STATE:
1. Parasite is a low-virulence
strain
2. Inoculation into the host is
low
3. Patient’s immune system
is intact
SYMPTOMATIC INTESTINAL
AMEBIASIS
1. Amebic colitis
2. Amebic dysentery
SYMPTOMATIC
EXTRAINTESTINAL
AMEBIASIS:
1. Abscess
2. Amebic pneumonitis
3. Cough, weakness, weight
loss, sweating, sweating,
nausea and vomiting
4. Venereal amebiasis
Leading cause of
parasitic deaths after
only malaria
Thrives in subtropical
and tropical areas
Ingestion of the
infective stage, the
cyst, occurs through
hand-to-mouth
contamination and
food or water
contamination.
Unprotected sex,
vectors (e.g. flies and
cockroaches) and
improperly treated
water supplies are
possible source of
infection.
TREATMENT:
paromomycin, diloxanide
furoate (Furamide),
or metronidazole (Flagyl) →
asymptomatic
iodoquinol, paromomycin, or
diloxanide
furoate → symptomatic
intestinal amebiasis
Metronidazole or tinidazole →
extraintestinal amebiasis
PREVENTION AND
CONTROL
Boiling water with
iodine crystals
(infective
(quadrinucleated)
cyst is
resistant to routine
chlorination)
filtration and
chemical treatment
of water
properly washing
food products
avoiding the use of
human feces as
fertilizer
goof personal and
sanitation practices
protection of food
from flies and
cockroaches
avoidance of
unprotected sexual
practices
AMOEBA
Entamoeba hartmanni
MORPHOLOGY
LABORATORY
DIAGNOSIS
Examining stool
Use of ocular
micrometer is
needed for size
identification
EPIDEMIOLOGY
Geographic
distribution is
cosmopolitan
ingestion of infected
cysts
present in
contaminated food or
water accounts
for the transmission of
E. hartmanni
CLINICAL
SYMPTOMS
ASYMPTOMATIC
TREATMENT
- Nonpathogen
- Treatment not
indicated
PREVENTION
AND CONTROL
Good sanitation
and personal
hygiene
practices
Protection of
food from flies
and cockroaches
AMOEBA
Entamoeba coli
MORPHOLOGY
LABORATORY EPIDEMIOLOGY
DIAGNOSIS
Stool
Found worldwide
examination
Occurs in cold climates
Geographic areas that
have poor hygiene and
sanitation practices
Transmitted through the
ingestion of the infected
cyst through
contamination food or
drink
CLINICAL SYMPTOMS
ASYMPTOMATIC
TREATMENT
- Nonpathogenic
- Not indicated
PREVENTION AND
CONTROL
adequate disposal of
human feces
proper personal
hygiene practices
Protection of food
and drink from flies
and cockroaches
AMOEBA
Entamoeba polecki
MORPHOLOGY
LABORATORY
DIAGNOSIS
Stool samples
EPIDEMIOLOGY
Considered a parasite
of pigs and monkeys
Human infections are
relatively rare
Ingestion of this cyst is
most likely responsible
for the onset of
infection
CLINICAL
SYMPTOMS
ASYMPTOMATIC
Discomfort
associated –
diarrhea
TREATMENT
- Metronidazole
(flagyl) and
diloxanide
furoate
(Furamide)
PREVENTION
AND CONTROL
Improving personal
hygiene and
sanitation process
AMOEBA
Endolimax nana
MORPHOLOGY
LABORATORY
DIAGNOSIS
Stool samples
EPIDEMIOLOGY
Warm, moist regions
CLINICAL
SYMPTOMS
ASYMPTOMATIC
Poor hygiene and
TREATMENT:
substandard sanitary - nonpathogen
conditions
Contaminated food
and water
PREVENTION
AND CONTROL
Protection of food
and drink from
flies and
cockroaches
Good sanitation
and personal
hygiene
AMOEBA
Iodamoeba butschlii
MORPHOLOGY
LABORATORY
DIAGNOSIS
EPIDEMIOLOGY
Stool samples
Higher prevalence in
tropical regions than in
temperate regions
Method of diagnosis:
1. fecalysis
2. concentration
techniques
3. molecular
techniques
iodine wet preps –
benefits in identifying
cysts
glycogen mass remains
unstained following
trichrome staining
Lower frequency in
transmission of E. coli
and E. nana
Transmission of I.
bütschlii occurs when
the infective cysts are
ingested in
contaminated
food or drink.
Hand-to-mouth
transmission may
also occur
CLINICAL
SYMPTOMS
PREVENTION
AND
CONTROL
Nonpathogenic Personal
hygiene and
Does not
sanitation
produce
clinical
symptoms
AMOEBA
MORPHOLOGY
Entamoeba gingivalis
LABORATORY
DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOG
Y
CLINICAL
SYMPTOMS
Mouth scrapings
Lives around
the gum line
of the teeth in
the tartar and
gingival
pockets
Contracted via
mouth-to-mouth
Infections in the
mouth and in the
genital tract produce
no symptoms
Material from
the tonsillar
crypts and
pulmonary
abscess
Sputum
No known cyst stage
Vaginal and
cervical material
Its
trophozoites
inhabit
tonsillar
crypts and
bronchial
mucus
Trophozoites
feed on
disintegrated
cells and
multiply by
binary fission
Higher
chance of
infection to
women who
have IUDs
Droplet
contamination
(transmitted
through
contaminated
drinking utensils)
Nonpathogenic E.
gingivalis trophozoites
are frequently
recovered in patients
suffering from
pyorrhea alveolaris.
do not produce
symptoms of their own
TREATMENT:
- not indicated
(nonpathogenic)
PREVENTI
ON AND
CONTROL
Proper care
of the teeth
and gums
Prompt
removal of
IUDs
AMOEBA
MORPHOLOGY
Naegleria fowleri
LABORATORY
DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY CLINICAL
SYMPTOMS
Cerebrospinal
fluid (saline and
iodine wet
preps)
Ameboid
trophozoites of
N. fowleri are
the
only form known
to exist in
humans.
Warm bodies of
water (e.g. lakes,
streams, ponds
and swimming
pools)
Samples of
tissue and nasal
discharge
CYST:
- 9 to 12 µm
- generally round and have thick cell
walls
- one nucleus with a large centrally
located karyosome (no peripheral
chromatin)
- granular and with vacuole
cytoplasm
May be cultured
(has trailing
effect when
placed on agar
plates that have
been previously
inoculated with
gram-negative
bacili
Replicate by
binary fission
Trophozoites
converting to
cysts and
flagellates and
then
back to amebic
trophozoites,
occurs in the
external
environment
Contaminated
ducts
Nasal mucosa
In the passages →
Asymptomatic
PAM → invade the
brain → rapid
tissue destruction.
Symptoms: fever,
headache, sore
throat, nausea, and
vomiting. Stiff neck
and seizures, smell
and taste
alterations, blocked
nose and Kernig’s
sign. 3-6 days after
onset → death.
TREATMENT:
Amphotericin B,
rifampin, or
miconazole.
PREVENTION
AND
CONTROL
Total
eradication is
highly unlikely
Posting offlimits signs
Educating the
medical
community
Chlorination of
pools and hot
tubs
AMOEBA
Acanthamoeba species
MORPHOLOGY
LABORATORY
DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY
CLINICAL
SYMPTOMS
CSF examination,
brain tissue
Acquired by:
1. aspiration
or nasal
inhalation
2. direct
invasion of
the parasite
in the eye
(affects
those who
wear
contact
lenses and
those who
have
experience
d trauma to
the cornea)
Primarily occur in
patients who are
immunocompromise
d or debilitated
Granulomatous
amebic
encephalitis:
- headaches
- seizures
- stick neck
- nausea
- vomiting
- granulomatous
lesions
Corneal scrapings
→ choice of
recovery (eye)
[may be cultured
on non-nutrient
agar plates
seeded with
gram-negative
bacteria]
Indirect
immunofluorescen
t → choice for
speciating
Method of
diagnosis:
1. microscopy
2. culture
methods
(NNA lawned
with E. coli)
3. molecular
methods
Migrate through
hematogenous
spread and
invade the CNS
Acanthamoeba
keratitis →
serious eye
infections that is
cause by
contact lenses
who use homemade,
nonsterile saline
solutions
Immunocompromise
d animals appear to
contract fatal CNS
infections
Acanthamoeba
keratitis:
- amebic
keratitis
- sever ocular
pain
- vision
problems
- perforation of
the cornea
TREATMENT:
- sulfamethazine
, itraconazole,
ketoconazole,
miconazole,
propamidine
isethianate,
and rifampin.
PREVENTIO
N AND
CONTROL
Follow
manufacturerestablished
protocols
Nonsterile
saline
solutions
BACKGROUND
- Phylum protozoa
- Subphylum Mastigophora
MORPHOLOGY
- FLAGELLA – responsible for its movement (whiplike
structures)
- All flagellate life cycles consist of the trophozoite form
- Those with no known cyst stage – more resistant to
destructive forces, surviving passage into the stomach
following ingestion
- Reside mainly in the small intestine, cecum, colon and
duodenum
- FLAGELLATE CYSTS – equipped with thick, protective
cell walls (may survive in the outside environment)
LABORATORY DIAGNOSIS
- Stool examination
- TROPHOZOITES – loos, liquid, or soft stool
- CYSTS – formed stools
- Presence of either or both flagellate morphologic forms
is diagnostic
- Parts that help with flagellate identification:
1. AXOSTYLE – a rodlike support structure found in
some flagellates
2. Undulating membrane
- Flagellate trophozoites – flagella is not always visible
- Stains used:
1. Saline
2. Iodine wet preparations
3. Permanent stains
PATHOGENESIS AND CLINICAL SYMPTOMS
- Often recovered from patients suffering from diarrhea
without an apparent cause
- Pathogenic flagellates have transmission routes similar
to those of the non-pathogenic variety
- G. intestinalis – the only intestinal flagellate, pathogenic
Flagellate
Giardia
intestinalis
Morphology
Lab diagnosis
Stool examination
Shed in showers –
many organisms may
be passed and
recovered on one
day’s sample and the
ff day’s sample ay
reveal no parasites at
all
Multiple samples is
recommended
Tests used:
1. Enterotest (string
test)
2. duodenal
contents (by
aspiration)
3. upper small
intestine biopsies
4. Fecal antigen
detection by
enzyme
immunoassays
(EIA)
5. enzyme linked
immunosorbent
assay (ELISA)
6. Direct
fluorescence
7. Giardia Western
immunoblotting
8. RT-PCR
Life cycle notes
epidemiology
Symptoms/treatment
Cyst enters the
stomach → gastric
acid stimulates cysts
to excyst in the
duodenum →
trophozoites become
established and
multiply (8 hrs) by
longitudinal binary
fission → feed by
attaching their
sucking disks to the
mucosa of the
duodenum
Found in lakes, streams,
and other water sources
Only known pathogenic intestinal
flagellate
Major cause of parasitic
diarrheal outbreaks in
the US
Asymptomatic carrier state –
asymptomatic
Trophozoites may
also infect the
common bile duct
and gallbladder
Cysts are viable for 3
months in water
Trophozoites
disintegrate quickly
when entered the
outside environment
Cysts – resistant to
routine chlorination
Filtration and chemical
treatment should be
done for drinking water
Transmitted by eating
contaminated
fruits/veggies
Person-to-person
contact through oralanal sexual practices or
fecal-oral route
High risk of those in day
care centers, people
living in poor sanitary
conditions and those
who practice
unprotected sex
Giardiasis (traveler’s diarrhea)
- Mild diarrhea, abdominal
cramps, anorexia, and
flatulence to tenderness of
the epigastric region,
steatorrhea, and
malabsorption syndrome
- Light colored stools w/ high
fat content
- Fat-soluble vitamin
deficiencies, hypoproteinemia
with hypogammaglobulinemia
and structural changes in
intestinal villi
Incubation period: 10-36 days
TREATMENT:
1. Metronidazole (Flagyl)
2. Tinidazole (Tindamax)
3. Nitazoxanide (Alinia)
Prevention and
control
Proper water
treatment
(chemical therapy
and filtration)
Good personal
hygiene
Proper cleaning
Cooking of food
Avoidance of
unprotected oralanal sex
Double-strength
saturated iodine
solution may be
added to potentially
contaminated
water
Flagellate
Chilomastix mesnili
Morphology
Lab diagnosis
Epidemiology
Trophozoites –
freshly passed
liquid stools
Found in warm
climates
Cysts – formed
stools
Both –
semiformed
consistency
Stain: iodine wet
prep
Transmission –
ingestion (hand-tomouth
contamination or
contaminated food
or drink)
Symptoms/treatment Prevention
and control
Asymptomatic
Good personal
hygiene
Good public
sanitation
Flagellate
Morphology
Dientamoeba
fragilis
Lab diagnosis
Life cycle notes
epidemiology
Symptoms/treatment
Stool samples
Reside in the
mucosal crypts
of the large
intestine
Exact mode of
transmission is
unknown
Asymptomatic carrier
state: Asymptomatic
Multiple samples as
amount of parasite
shedding may vary
form day-to-day
Has the ability to
blend in well with the
background material
RT-PCR – most
sensitive of
diagnostic methods
No known cyst stage
Rarely known to
ingest RBC
Those who are at
risk of contracting:
1. Children
2. Homosexual
men
3. Those living in
semicommunal
groups
4. People who
are
institutionalized
Symptomatic: diarrhea,
abdominal pain,
bloody/mucoid stools,
flatulence, nausea,
vomiting, weight loss,
fatigue or weakness,
constipation, low-grade
eosinophilia, and
pruritus
TREATMENT:
Iodoquinol or
Paromomycin
(humatin)
Prevention and
control
Good personal
and public
sanitary
conditions
Avoidance of
unprotected
homosexual
practices
Eradication of
the helminth
eggs
Flagellate
Morphology
Trichomonas hominis
Lab diagnosis
Life cycle notes
Symptoms/treatment
Stool samples
Found in warm and temperate
Asymptomatic
Children appear to contract this
more often than adults
No treatment indication
Prevention and
control
Improved personal
and public sanitary
practices
Transmission: ingesting
trophozoites (mostly
contaminated milk) and fecaloral transmission
No known cyst stage
Flagellate
Enteromonas hominis
Morphology
Lab diagnosis
Life cycle notes
Symptoms/treatment
Stool samples
Found in warm and
temperate
Asymptomatic
Transmission:
ingesting of
infected cysts
No treatment
indication
Prevention
and control
Proper
personal
hygiene
Flagellate
Retortamonas intestinalis
Morphology
Lab diagnosis
Life cycle notes
Symptoms/treatment
Stool samples
Found in warm and temperate
Asymptomatic
Transmission: ingestion of
infected cysts
No treatment indication
Prevention
and control
Improved
personal and
public sanitary
practices
Flagellate
Morphology
Trichomonas tenax
Lab diagnosis
Life cycle notes
Symptoms/treatment
Mouth scrapings
(tartar between the
teeth and gingival
margin)
trophozoites survive in the
body as mouth scavengers
that feed primarily on local
microorganisms.
Invades respiratory
tract (but affects those
who have underlying
disease)
multiply by longitudinal binary
fission.
No notable symptoms
unable to survive the digestive
process
Flagellate
Morphology
Trichomonas vaginalis
No known cyst stage
No treatment indication
Lab diagnosis
Life cycle notes
Symptoms/treatment
spun urine, vaginal
discharges, urethral
dis charges, and
prostatic secretions.
reside on the mucosal
surface of the vagina in
infected women
Persistent Urethritis: enlarged tender
prostate, dysuria, nocturia, and
epididymitis. Thin, white urethral
discharge
Saline wet
preparations
Persistent Vaginitis: a foul-smelling,
greenish-yellow liquid vaginal discharge
after an incubation period of 4 to 28
days. Burning, itching, and chafing,
thrive in a slightly alkaline Urethral
or slightly acidic pH
involvement, dysuria, and increased
environment, such as
frequency of urination
that commonly seen in
an
Infant infections: recovered from infants
unhealthy vagina.
suffering from both respiratory infection
and conjunctivitis.
Male: prostate gland
region and the epithelium Metronidazole (Flagyl)
of the urethra
Other tests: phase
contrast microscopy,
Papanicolaou (Pap)
smears, fluorescent
stains,
monoclonal antibody
assays, enzyme
immunoassays, and
cultures. InPouch TV
culture system
multiply by longitudinal
binary fission and feed
on local bacteria and
leukocytes
Prevention
and control
Good oral
hygiene
Prevention
and control
Avoid
unprotected
sex
avoidance of
sharing douche
equipment
and communal
bathing, and
close contact
with potentially
infective
underclothing,
toilet
articles, damp
towels, and
wet sponges
HEMOFLAGELLATES
• Members of the clinically
significant group of parasites
located in blood and tissue that
move by means of flagella, known
as the hemoflagellates, belong to
the genera Leishmania and
Trypanosoma.
body length, forms into a free
flagellum at the anterior end of the
epimastigote.
FOUR MORPHOLOGIC FORMS:
Amastigotes - measures 5 by 3 μm in
size. contains a nucleus, a basal body
structure (called a blepharoplast), and
a small parabasal body. Kinetoplast is
an umbrella term often used to refer
to the blepharoplast and small
parabasal body.
Promastigotes - measures 9 to 15 μm
in length. large single nucleus is
located in or near the center of the
long slender body. The kinetoplast is
located in the anterior end of the
organism. A single free flagellum
extends anteriorly from the axoneme.
Epimastigotes – measures
approximately 9 to 15 μm in length.
Body is slightly wider than
promastigote. The single nucleus is
located in the posterior end of the
organism. The kinetoplast is located
anterior to the nucleus. An undulating
membrane, measuring half the
• Leishmaniasis is a general term
used to describe diseases caused
by the hemoflagellate genus
Leishmania.
• Diseases caused by Leishmania
spp. (e.g., Baghdad boils, bay sore,
chiclero ulcer, dum dum fever,
espundia, forest yaws, kala-azar,
oriental sore, pianbois, and uta).
Trypanosomiasis is a general term
used to refer to human diseases
caused by hemoflagellates of the
genus Trypanosoma. These diseases
have been well documented through
the ages. Ancient papyri discussed the
disease from veterinary and human
perspectives.
Morphological forms
AMASTIGOTES
PROMASTIGOTES
Morphology
EPIMASTIGOTE
TRYPOMASTIGOTES
Lab diagnosis
• Blood, lymph node and ulcer aspirations, tissue biopsies, bone marrow, and
cerebrospinal fluid (CSF) are the specimens of choice for diagnosing the
hemoflagellate morphologic forms. In addition, serologic and molecular tests
are also available for confirming the presence of these organisms.
Clinical symptoms
• symptoms associated with hemoflagellate infections range from a small red
papule at the infection site, with intense itching, secondary bacterial infections,
fever, and diarrhea, to kidney involvement, mental retardation, a comatose
state, and death. In some cases, the initial skin lesions spontaneously heal,
whereas in others they may remain dormant for months or even years.
Hemoflagellate
Leishmania
braziliensis
complex
Common associated
disease and condition
names:
Mucocutaneous
leishmaniasis, chiclero
ulcer, espundia, forest
yaws, pian bois, uta.
Morphology
Lab diagnosis
Life cycle
notes
Epidemiology
Symptoms / treatment Prevention
- specimen of choice
for identifying the
amastigotes of L.
braziliensis complex
is a biopsy of the
infected ulcer.
- Sandflies of the
genera Lutzomyia
and
Psychodopygus are
responsible for
transmitting the
promastigotes of
the species of the
L. braziliensis
complex into
unsuspecting
humans via a
blood
meal, resulting in a
skin bite.
- diagnostic stage
for the species of
the L. braziliensis
complex is the
amastigote.
- the amastigote
serves as
the infective stage
for the sandfly.
- ingestion,
during a blood
meal of an infected
human, the
amastigotes
transform back
into promastigotes
- composed of L.
braziliensis (found
from Mexico to
Argentina), L.
panamensis (found
in Panama and
Colombia), L.
peruviana (found in
the Peruvian Andes),
and L. guyanensis
(found in Guiana,
parts of Brazil, and
Venezuela).
Mucocutaneous
Leishmaniasis.
- Microscopic
examination of
the Giemsa-stained
preparations –
amastigote
- Promastigotes may
be
present when the
sample is collected
immediately
after introduction
into the patient.
- infected material,
which often
demonstrates the
promastigote stage,
and serologic
testing.
- Enzyme analysis
- also be found in
Ecuador, Bolivia,
paraguay, and other
Central and South
American countries,
particularly in the
rain forest regions,
where chicle sap for
chewing gum is
Harvested.
- Transmission is
generally through
the bite of the
Lutzomyia or
Psychodopygus
- occur within a few weeks
to months after
transmission into a
previously uninfected
human. Large ulcers in the
oral or nasal mucosa areas
(mucocutaneous)
- A cutaneous (meaning
affecting or relating to the
skin) lesion may heal
on its own. Untreated
cases – destruction of
nasal septum
- lips, nose, and other
surrounding soft parts may
also be affected in these
infections. Edema and
secondary bacterial
infections, combined with
numerous mucosal
lesions, may cause
disfigurement of the
patient’s face.
- Public
awareness
through
education
programs in
endemic areas
and exercising
personal
protection
against contact
with sandflies
(e.g., protective
clothing,
repellents,
screening)
- prompt
treatment and
eradication of
infected ulcers,
and control of
the sandfly
population and
reservoir
Hosts.
- Work to
produce a
vaccine against
members of
Leishmania
donovani complex
Common associated
disease and condition
names:
Visceral leishmaniasis,
kala-azar, dum dum
fever.
- Molecular
techniques
- Kinetoplast DNA /
scizodeme analysis
- Nuclear DNA
hybridization
- zymodeme analysis
in the fly midgut.
These
promastigotes
multiply
and the resulting
developed forms
eventually
migrate into the
salivary gland of
the fly, where
they are ready to
be transferred to a
new human
during a blood
meal.
- Montenegro skin
test (similar to
tuberculin skin test)
- identical to that
- Giemsa-stained
slides of blood, bone
marrow, lymph node
aspirates, and
biopsies of the
infected areas are
better choices
for demonstrating
the diagnostic
amastigote forms.
- Serologic
of L. braziliensis,
with only two
exceptions. First,
the specific sandfly
species
responsible for L.
donovani
transmission vary
with each of the
three subspecies.
- Second, L.
donovani primarily
affects the visceral
tissue of the
infected human.
- Death is usually
attributed to a secondary
bacterial infection.
Treatment:
- sodium stibogluconate
(Pentosam).
- liposomal amphotericin B
(Ambisome)
and oral antifungal drugs
such as fluconazole
(Diflucan),
ketoconazole(Nizoral) and
itraconazole (Sporonox).
- composed of L.
donovani (found in
India, Pakistan,
Thailand,
parts of Africa, and
the Peoples Republic
of
China), L. infantum
(found in the
Mediterranean
area, Europe, Africa,
the Near East, and
parts of the former
Soviet Union), and L.
chagasi (found in
Central and South
America). L.
donovani and
- Visceral Leishmaniasis.
- also known as kala-azar(
black fever) or dum dum
fever, often present with a
nondescript abdominal
illness and
hepatosplenomegaly
(enlargement of the spleen
and liver).
- may resemble malaria or
typhoid fever with the
development of fever and
chills. symptoms is gradual
and follows an incubation
the L. braziliensis
complex and
other Leishmania
spp. is ongoing,
with some
vaccines for
animals
(dogs) presently
in experimental
trials.
- Protection
against sandflies
by repellents,
protective clothing, and
screening are
essential measures to reduce
future L. donovani
complex
infections. Prompt
treatment of
human infections, as well as
control of the
sandfly population
and reservoir
hosts, will also
testing is available
using IFA (indirect
fluorescent
antibody), ELISA
(enzyme-linked
immunosorbent
assay), and DAT
(direct agglutination
test).
- person to person
via blood
transfusions.
-leishmaniasis
transmission arose
during and
following the Gulf
War.
L. infantum are
known to be
endemic in areas
of the Middle East,
including Yemen,
Oman,
Kuwait, Iraq, Saudi
Arabia, the United
Arab
Emirates, and
Bahrain.
period ranging from 2 weeks
to 18 months.
- Diarrhea, as well as anemia,
may often be present. weight
loss and emaciation, tend to
occur following parasitic
invasion of the liver
and spleen. a rare papule,
which mostly occurs at the
bite site, skin lesions are
absent. Advanced stages of
disease result in kidney
damage (e.g.,
glomerulonephritis,
inflammation of the
glomeruli of the kidney) and
granulomatous areas of skin.
A characteristic darkening of
the skin may be noted.
- Chronic cases leads to
death in 1 or 2 years. acute
disease debilitates the
patient and becomes
lethal in a matter of weeks.
TREATMENT:
- Liposomal amphotericin B
(Ambisome), Sodium
stibogluconate (Pentosam)
- use of gamma interferon
combined with pentavalent
antimony.
help halt the
spread
of disease.
Leishmania
Mexicana complex
Common associated
disease and condition
names: New World
cutaneous
leishmaniasis, chiclero
ulcer, bay sore.
- by demonstrating
the amastigote form
in Giemsa-stained
preparations of
lesion biopsy
material.
- Culture on NNN
medium
demonstrates the
promastigote
stage of these
organisms.
- Serologic testing
using
monoclonal
antibodies.
Schizodeme analysis,
zymodeme analysis,
and nuclear DNA
hybridization are
- The life cycle of
the members of
the L. mexicana
complex is
identical to that of
L. braziliensis. The
primary vectors
are sandfly species
of the genus
Lutzomyia.
- composed of L.
mexicana (found in
Belize, Guatemala,
and the Yucatan
peninsula), L. pifanoi
(found in the
Amazon River basin
and parts of Brazil
and Venezuela), L.
amazonensis (found
in the Amazon basin
of Brazil), L.
venezuelensis (found
in the
forested areas of
Venezuela), and L.
garnhami
(found in the
Venezuelan Andes).
Members of this
complex are often
- allopurinol (AIDS PATIENT)
- that HIV-infected persons
receive secondary prophylaxis as part of their
treatment plan.
- visceral leishmaniasis which include a
combination of paramomycin and miltefosine.
Neither of these drugs is
available in the United States
at this time.
- New World Cutaneous
Leishmaniasis. Also
known as bay sore and
chiclero ulcer, cutaneous
leishmaniasis usually
characterized by a single
pus-containing ulcer, which
is generally selfhealing.
- 40% of infections affect the
ear and can cause serious
damage to the
surrounding cartilage. of
anergic (the inability of an
individual to mount an
adequate immune response)
and hypersensitivity
immunologic responses,
spontaneous healing of the
ulcers does not occur.
- Protection
against sandflies
by repellents,
protective
clothing, and
screening are
essential
measures to
reduce future L.
mexicana
complex
infections.
Prompt
treatment of
human infections, as well as
control of the
sandfly and
reservoir host
populations, will
also help halt the
available on a
research basis.
transmitted by the
bite of
a Lutzomyia sandfly,
with forest rodents
serving
as the reservoir host.
- infections with L. pifanoi,
the initial lesion appears,
ulcerates or disappears and,
after a period of months to
years, appears in local and
distant areas from the bite
site with lepromatousappearing lesions. L.
amazonensis infections
have been known to
progress to an incurable
diffuse cutaneous form of
the disease. cutaneous
leishmaniasis usually occurs
when the patient is anergic.
TREATMENT:
- Pentavalent antimonials,
such as sodium stibogluconate (Pentosam),
Antimony combined with
pentoxifylline taken orally
three times a day for 30 days
has been shown to be
superior to antimony alone.
Amphotericin B and
liposomal amphotericin B
(Ambisome) have also
proven to be effective.
spread of
disease.
Leishmania tropica
complex
Common associated
disease and condition
names: Old World
cutaneous
leishmaniasis, oriental
sores, Delhi boils,
Baghdad boils, dry or
urban cutaneous
leishmaniasis.
- With the
exception of the
examination of
specific sandfly
Giemsa-stained
slides (reveal
species
amastigotes).
and the area of
the body most
- Culture of the
affected, the life
under of the ulcer
cycle of L. tropica
tissue may also
complex is
revels promastigote.
basically identical
to that of L.
- Serologic tests,
braziliensis. All
such as IFA testing,
three of the L.
are available.
Schizodeme analysis, tropica
zymodeme analysis, subspecies are
and nuclear DNA
transmitted by
hybridization are
the Phlebotomus
also available on a
sandfly. L. tropica
research basis.
complex
primarily
attacks the
human lymphoid
tissue of the skin.
- Microscopic
- protection by
the use of
L. tropica (found in
Leishmaniasis.
protective
the Mediterranean
region, Middle East,
clothing,
Old World leishmaniasis,
Armenia, Caspian
repellents, and
oriental sore, and Baghdad
region, Afghaniscreening are
or Delhi boil, cutaneous
stan, India, and
leishmaniasis is characterized essential to
Kenya), L. aethiopica
prevent future
by one or more ulcers
(found in the
containing pus that generally L. tropica
highlands of
self-heal.
complex
Ethiopia, Kenya, and
infections. In
Southern
- develop a small red papule, addition, the
Yemen), and L. major
located at the bite site,
prompt
(found in the desert
which is typically 2 cm or
treatment and
region of
larger in diameter and may
Turkmenistan,
eradication of
cause intense itching.
Uzbekistan, and
infected ulcers
Kazakhstan,
are crucial to
- On occasion, because of
Northern Africa, the
halt disease
anergic and hypersensitivity
Sahara, Iran, Syria,
transmission. A
immunologic responses,
Israel, and Jordan).
vaccine has
spontaneous healing of the
Members of this
ulcers does not occur. DCL
been
complex are often
occurs especially on the
developed and
transmitted by the
limbs and face when an
the preliminary
bite of the
immune response fails to
results are
Phlebotomus
take place.
promising;
sandfly, but the
reservoir hosts for
however, the
TREATMENT:
each of the three
clinical trials for
- effective treatment of L.
members of this
this vaccine are
tropica complex is sodium
complex differ
still ongoing.
stibogluconate (Pentosam).
- composed of
- Old World Cutaneous
The use of steroids,
application of heat to the
Trypanosoma
brucei gambiense
Common associated disease and condition
names: West African sleeping sickness, Gambian
trypanosomiasis.
T. brucei gambiense is found in the tropical
areas of western and central Africa. Commonly
called West African sleeping sickness or Gambian
trypanosomiasis.
acquired through blood transfusion, organ transplantation, and congenital transmission (from
pregnant mother to fetus).
- Blood, lymph node - infected with T.b.
aspirations, and CSF
are the specimens of
choice for
diagnosing T.b.
gambiense.
- Giemsa-stained
slides of blood and
lymph node
aspirations from
infected patients
reveal the typical
trypomastigote
morphologic forms.
- CSF—microscopic
examination of the
sediment for
trypomastigotes,
detection of the
presence of
immunoglobulin M
(IgM), and detection
of the
gambiense
following the
injection of
trypomastigotes by
the tsetse fly
during its blood
meal. The entering
trypomastigotes
migrate through
the bloodstream and into
the lymphatic
system,
multiplying by
binary fission.
- invasion of the
CNS may occur.
The
trypomastigotes
are transmitted
back to the tsetse
fly vector when it
feeds on an
- found in tropical
West Africa
and Central Africa,
especially in shaded
areas along stream
banks where the
tsetse fly vector
breeds. The two
species of tsetse flies
responsible for the
transmission of T.b.
gambiense are
Glossina palpalis and
Glossina tachinoides.
There are no known
animal reservoir
hosts.
infected lesions, meglumine
antimonate (Glucantime),
pentamidine, and oral
ketoconazole may be
indicated for treating L.
tropica complex infections.
Paromomycin ointment may
also be given to aid in
healing.
- West African (Gambian)
Sleeping Sickness.
- West African sleeping
sickness begin to occur after
an asymptomatic
incubation period of a few
days to several weeks.
- painful chancre (ulcer), surrounded by a white halo at
the bite site. Fever, malaise,
headache, generalized
weakness, and anorexia are
often experienced when the
trypomastigotes settle into
the lymphatic system.
lymph node enlargement
(lymphadenopathy) may be
apparent during this time.
- Winterbottom’s sign refers
to the enlargement of the
cervical lymph nodes. in
reference to this
trypanosomal disease. Other
- destroying their
breeding areas
via chemical
treatment and
clearing of brush.
Proper
protective
clothing,
repellents, and
screening, as
well as prompt
treatment of
infected persons,
presence of
proteins. Infected
patients typically
have high levels of
both IgM and
proteins in their CSF.
In addition, serum
IgM testing may be
indicated. The
presence of IgM in
serum and/or CSF is
generally considered
diagnostic. A
number of
serologic tests are
also available.
infected human.
Once ingested by
the tsetse fly, the
trypomastigotes
continue to multiply and eventually
migrate back to
the salivary gland,
converting into
epimastigotes
along the way.
Once in the
salivary gland, the
epimastigotes
transform back
into
trypomastigotes,
thus completing
the cycle.
symptoms that may be seen
during the glandular phase of
the disease include
erythematous
(red) rash, pruritis, localized
edema (swelling),
and Kerandel’s sign (a
delayed sensation to
pain). In patients in whom
the central nervous system
(CNS) becomes involved,
mental retardation, tremors,
meningoencephalitis,
somnolence (excessive
sleepiness), and character
changes may
develop. In the final stage of
disease, the patient
slips into a coma and death
occurs.
TREATMENT:
- melarsoprol, suramin,
pentamidine, and
eflornithine. The treatment
of choice is situation
dependent and is dictated by
a number of factors,
including patient age (adult,
child), stage of disease, and
whether the patient is
pregnant at
the time.
Trypanosoma
brucei
rhodesiense
Common associated disease and condition
names: East African sleeping sickness, Rhodesian
trypanosomiasis. Trypanosoma brucei
rhodesiense is found in eastern and central
Africa. Commonly called East African sleeping
sickness or Rhodesian trypanosomiasis, the
disease course for the illness caused by this
organism is much more aggressive
than that of its West African counterpart.
- detection of
the typical T.b.
rhodesiense
trypomastigotes are
blood slides stained
with Giemsa and
microscopic
examination of CSF
sediment. Protein
and IgM studies on
CSF may also be
performed. As
with T.b. gambiense,
the presence of IgM
in the CSF is
diagnostic for T.b.
rhodesiense.
- only difference in
the life cycles of
T.b. rhodesiense
and T.b.
gambiense are the
species of tsetse
fly vector. The two
primary species of
tsetse fly vectors
responsible for
transmitting T.b.
rhodesiense are
Glossina morsitans
and Glossina
pallidipes.
Additional species
noted for attacking
game animals may
also transmit this
organism.
- found in East and
- East African (Rhodesian)
Central Africa,
especially in brush
areas. Cattle and
sheep, as well as
wild game animals,
are known
reservoir hosts of
this organism.
Sleeping Sickness.
- much more virulent
organism than T.b.
gambiense. Following a short
incubation period, patients
suffering from acute East
African sleeping sickness
experience fever,
myalgia, and rigors.
Winterbottom’s sign may or
not be present.
Lymphadenopathy is absent.
Rapid weight loss is common
and the CNS becomes
involved early in the disease
course. In addition, mental
disturbance, lethargy, and
anorexia may also be
present.
- Death, in part caused by
subsequent kidney damage
(glomerulonephritis) and
myocarditis (inflammation
of the heart), usually occurs
within 9 to 12 months in
untreated patients.
TREATMENT:
Identical to T.b gambiense
- extremely early
treatment
is crucial to halt
further
transmission of
the
disease.
Additional
measures
include prompt
medical
treatment of
infected
domestic
animals,
as well as
protective
clothing,
screening, and
repellents.
- breeding may
occur wherever
brush is
abundant,
primarily
away from water
sources,
complicates
prevention and
control efforts.
The clearing of
brush
areas and control
of the tsetse fly
population may
reduce the risk
of future disease
transmission.
Trypanosoma cruzi Common associated disease and condition
names: Chagas’ disease, American
trypanosomiasis. Trypanosoma cruzi is found in
southern portions of the United States, Mexico,
and Central and South America. Commonly
referred to as Chagas’ disease or American
trypanosomiasis, the disease course for this
illness often presents itself with cardiac and
gastrointestinal
distress.
endemic areas of South America is known as
xenodiagnosis.
- Giemsa-stained
blood slides are the
specimen of choice
for detection of the
typical T. cruzi
trypomastigotes.
Epimastigotes may
rarely be seen in the
circulating blood;
however, this form is
primarily found only
in the arthropod
vector. Lymph node
biopsy Giemsastained slides, as
well as blood
culture, may reveal
the typical
amastigotes.
- most frequently
transferred to a
human host when
a reduviid bug
vector defecates
infective
trypomastigotes
near the site of its
blood meal.
- the bite produces
an itching
sensation in the
host. As the host
scratches
the bite area, the
trypomastigotes
conveniently
gain entry into the
host by literally
being rubbed into
the bite wound.
- complement
fixation (CF), DAT,
and indirect
immunofluorescence - blood
(IIF), polymerase
transfusions,
chain reaction (PCR) sexual intercourse,
- found primarily in
South and Central
America and only
rarely in North
America. The
highest known
prevalence of
disease is in Brazil.
- Although first
isolated in a
Panstrongylus
megistus, there are
additional reduviid
bug species that may
serve as vectors. Also
known as the
kissing bug,
conenose bug, and
triatomid bug,
the reduviid bug
nests in human
homes that are
open in design.
Although there are a
number of known
- Chagas’ Disease.
- asymptomatic, chronic, or
acute in nature. The most
common initial symptom is
the development of an
erythematous nodule, known
as a chagoma, at the site of
infection produced by the
proliferation of the T. cruzi
organisms.
- most frequently located on
the face. Edema as well as a
rash around the eyes and
face may subsequently
occur. The painful chagoma
may last 2 to 3 months
before subsiding. Patients
who contract T. cruzi
through the ocular mucosa
develop a characteristic
conjunctivitis and unilateral
edema of the eyelids, a
condition known as
Romaña’s sign.
- eradication of
reduviid bug
nests and the
construction of
homes without
open design are
crucial
measures
necessary to
help alleviate
the future
spread of the
disease. DDT
has proved to
be useful, not
only to control
the reduviid
population but
also to
decrease the
incidence of
malaria.
- bug infested
homes.
and ELISA testing
methods
transplacental
transmission,
and entry through
the mucous
membranes when
the bug bite is near
the eye or mouth.
- trypomastigotes
invade
surrounding cells,
where they transform into
amastigotes. The
amastigotes
proceed to
multiply, destroy
the host cells, and
then convert back
into
trypomastigotes.
The resulting
trypomastigotes
migrate through
the blood,
penetrate
additional cells in
the body, and
transform back
into amastigotes,
and the replication
and destruction
cycle repeats. A
number of areas in
mammalian hosts,
dogs and cats are
of particular
importance as
reservoir hosts in
Brazil.
- Chronic Chagas’ disease
may occur after the
initial diagnosis of an acute
disease or years to
decades after being initially
asymptomatic.
- myocarditis, enlargement
of the colon (sometimes
referred to as megacolon)
and esophagus
(sometimes referred to as
megaesophagus), and
hepatosplenomegaly. In
addition, CNS involvement,
cardiomegaly (enlargement
of the heart), and
electrocardiographic changes
may be seen. Complete
blockage of the heart, as well
as brain damage, may result,
causing sudden death.
- acute Chagas’ disease
typically experience fever,
chills, fatigue, myalgia,
and malaise. An attack of
acute infection may
result in one of the following
scenarios: (1) recovery; (2)
transition to the chronic
stage of disease; or (3)
death, which usually occurs a
few weeks after the attack.
Educational
programs
designed to
inform people,
especially in
endemic areas,
of the disease,
its
transmission,
and possible
reservoir hosts.
Developing
vaccine would
help
the body may
become infected,
including the
heart muscle, liver,
and brain.
- trypomastigotes
are transmitted
back to the
reduviid bug when
it feeds, via a
blood meal, on an
infected human.
On ingestion,
the
trypomastigotes
transform into
epimastigotes in
the midgut.
Multiplication of
the epimastigotes
produces
thousands of
additional
parasites that
convert back into
trypomastigotes
when they reach
the hindgut. These
trypomastigotes
are then passed
with the feces
when the bug
The frequency and form of
Chagas’ disease seen in small
children versus older
children and adults vary. In
general, Chagas’ disease is
most commonly seen in
children younger than 5
years.
TREATMENT:
- nifurtimox (Lampit). Other
medications include
benznidazole, allopurinol,
and the antifungal agent ketoconazole.
Trypanosoma
rangeli
Common associated disease and condition
names: None known. Trypanosoma rangeli is
found in many of the same geographic regions as
T. cruzi. There are presently no common names
known for disease caused by this organism.
Infections are generally asymptomatic and tend
to show no pathologic changes or signs of
disease.
- Giemsa-stained
blood slides are the
specimen of
choice for the
detection of the
typical T. rangeli
trypomastigotes. T.
rangeli
trypomastigotes can
be seen in the
peripheral blood
throughout the
course of the illness.
It can also be
diagnosed by
xenodiagnosis and
serologic testing
methods.
PCR-based methods
are also available.
defecates near the
site of its next
blood meal, and
thus the cycle
begins again.
- similar to that of
T. cruzi. The vector
responsible for
transmitting T.
rangeli is the
reduviid bug,
Rhodius prolixus.
- This vector
actually transmits
the parasitic
infection via its
saliva. T. rangeli
can be viewed in
the blood
throughout the
course of the
infection.
- commonly found in
the same geographic areas as T.
cruzi—regions of
South and Central
America, particularly
in the areas surrounding Brazil,
Venezuela,
Colombia, Panama,
El Salvador, Costa
Rica, Honduras, and
Guatemala. Its
vector, Rhodius
prolixus, is attracted
to the same open
house design as
other reduviid bug
species. It has
numerous reservoir
hosts such as
monkeys, raccoons,
dogs, cats,
armadillos, and
rodents.
- Patients infected by T.
rangeli are generally
asymptomatic and
demonstrate no evidence of
illness. It is generally thought
to be a benign infection.
TREATMENT:
- Nifurtimox and
benzimidazole
- Prevention
and control
measures for
T. rangeli
are the same
as those for
T. cruzi.
-
6.1 BACKGROUND
- Phylum Apicomplexa
- Class Aconoidasida
- Order haemosporida
- Plasmodium 10 species infect humans
1. P. vivax
2. P. ovale
3. P. malariae
4. P. falciparum
5. P. knowlesi
- Babesia 4 species infect humans
1. B. microti
2. B. divergens
- FORMS:
1. Ring form (early trophozoite)
- Ring like appearance
- Consist of blue cytoplasmic circle connected to a
red chromatin dot
- Has a vacuole
2. Developing trophozoite
- Remnants of the cytoplasmic circle and chromatin
dot
- Pigment (brown) is visible
3. Immature schizont
- Visible cytoplasmic material
- Active in chromatin replication
- Pigment granules (brown) is visible
4. Mature schizont
- Fully developed stage of merozoites
- Cytoplasmic material is not visible
5. Microgametocyte
- Round in shape (except P. falciparum)
- Pink to purple large diffuse chromatin mass
surrounded by colorless halo
6. Macrogametocyte
- Round to oval shape (except P. falciparum)
- Compact chromatin mass surrounded by
cytoplasmic material
- LIFE CYCLE NOTES
- ANOPHELES responsible for the transmission of
malaria to humans via a blood meal
- Transfers the infective stage of the parasite known
as sporozoites from its salivary gland into the
human bite wound
- Schizogony occurs (asexual multiplication)
- EXOERYTHROCYTIC CYCLE (reproduction
outside RBC) occurs from 8-25 days
- HYPNOZOITES dormant Plasmodium-infected
liver cells
- GAMETOCYTES transmission of the parasite
back into the vector occurs when the mosquito
ingests mature male (micro) and female (macro)
sex cells
-
ZYGOTE fertilized cell that was formed when the
male and female gametocytes unite in the
(aka ookinete)
OOCYST encysted and mature zygote
6.2 LABORATORY DIAGNOSIS
- Giesma-stained peripheral blood films specimen of
choice for the laboratory diagnosis
- Serologic tests
- PCR tests
- Thick blood smears for screening
- Thin blood smears for differentiating
- Blood films to be studied under oil immersion
- The greatest number of parasites is present in the
blood in between characteristic bouts of fever and chills
resulting from the release of merozoites and toxic
waste products from infected RBCs aka PAROXYSMS
- Blood collection every 6-12 hours for up to 48 hrs
before considering a patient to be free of Plasmodium
spp. Parasites
ANOPHELES SPP.
- Carrier of the plasmodium parasite
BABESIA SPECIES
6.3 PATHOGENESIS AND CLINICAL SYMPTOMS
- PAROXYSMS - once the erythrocytic phase is initiated
and large numbers of rupturing RBCs simultaneously
occur, the resulting merozoites and toxic waste
byproducts in the blood system produce the first clinical
symptom
- RIGOR a paroxysm is characterized by chills (lasts
about 10-15 mins)
- RECRUDESCENCE occurs when patients become
reinfected with rupturing with rupturing hypnozoites
months to years after the initial infection
- OTHER SYMPTOMS:
a. Headache
b. Lethargy
c. Anorexia
d. Ischemia
e. Nausea
f. Vomiting
g. Diarrhea
h. Anemia
i. CNS involvement
j. Nephrotic syndrome
- May mimic a number of other diseases
a. Meningitis
b. Pneumonia
c. Gastroenteritis
d. Encephalitis
e. Hepatitis
-
-
-
-
SEXUAL occurs within its tick
ASEXUAL occurs within its host
generally transmitted through the bite of an infected tick
of the genus Ixodes.
The ookinete travels to the salivary glands where
sporogony the process of spore and sporozoite
production via sexual reproduction takes place,
resulting in numerous sporozoites that can be
transmitted to a new host
LABORATORY DIAGNOSIS
- Giemsa-stained peripheral blood films
- Wright
- Thick and thin blood films
- Thin differentiate
- All blood films should be studied under oil
immersion
- serologic tests
- PCR techniques
PATHOGENESIS AND CLINICAL SYMPTOMS
- 1 to 4 weeks prior to the onset of symptoms.
- prodrome-like symptoms fever, headache, chills,
sweating, arthralgias, myalgias, fatigue, and
weakness.
- Hepatosplenomegaly and mild to severe hemolytic
anemia
- Elevated bilirubin and transaminase levels
- worse for the splenectomized and
immunocompromised patient.
B. divergens
- EPIDEMIOLOGY
- VECTOR Ixodes dammini
- Principal reservoir host Peromyscus
leucopus
- Found in European countries
- Transmission vector Ixodes Ricinus
- CLINICAL SYMPTOMS
- B. divergens tends to be the more severe of
the two parasitic infections and is frequently
fatal if left untreated.
-
-
-
B. microti tends to be rather benign and selflimiting.
- Disease with either of these organisms is
often more severe for older adult,
immunosuppressed, and/or splenectomized
patients.
TREATMENT
- Diminazene and pentamidine, in combination
or singly, and pyrimethamine and quinine, in
combination or singly
PREVENTION AND CONTROL
- avoid tick infested areas.
- tick must feed for at least 12 hours before it is
able to transmit the parasite.
- Using insect repellents
- eradicating the tick population
PARASITE
P. vivax
Benign
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE NOTES
Thin blood films
diagnosis
Invade young RBCs
(as they are pliable)
Thick blood films
Distortion of the
RBCs
tertian
malaria
Vivax malaria
Observe during
halfway between
paroxysms
EPIDEMIOLOGY CLINICAL SYMPTOMS /
TREATMENT
Tropics and
BENIGN TERTIAN MALARIA
subtropics
- 10-17-day incubation period
postexposure
Temperate
- Nausea, vomiting, headache,
regions
muscle pains and photophobia
- Paroxysms every 48 hours
- When chronic may damage
brain, liver, and kidney
TREATMENT
- quinine, quinidine, chloroquine,
amodiaquine, primaquine,
pyrimethamine, sulfadoxine,
dapsone, mefloquine,
tetracycline, doxycycline,
halofantrine, atovaquone,
proguanil, ginghaosu, artemisinin,
artemether, artesunate,
pyronaridine, Fenozan B07,
trioxanes, nonane endoperoxides,
azithromycin, and WRZ38605.
PREVENTION AND
CONTROL
Personal protection
netting, screening,
protecting clothing and
repellents
Prophylactic treatment
Avoidance of sharing IV
needles
Thorough screening of
donor blood
PARASITE
MORPHOLOGY
P. ovale
Benign
LAB DIAGNOSIS
Thin blood films
speciate
tertian
malaria
Thick blood films
presence
Mature schizont
choice for
examination
Note may develop ragged cell walls in
response to the growing parasite
LIFE CYCLE
NOTES
Invade young
RBCs (as they
are pliable)
EPIDEMIOLOGY CLINICAL SYMPTOMS / TREATMENT
Tropical Africa
Asia
South America
BENIGN TERTIAN MALARIA AND
OVALE MALARIA
- paroxysm (every 48 hours)
- relapses caused by reactivation of
hypnozoites
- infections that last approximately
1 year
TREATMENT
- quinine, quinidine, chloroquine,
amodiaquine, primaquine,
pyrimethamine, sulfadoxine,
dapsone, mefloquine, tetracycline,
doxycycline, halofantrine,
atovaquone, proguanil,
ginghaosu, artemisinin,
artemether, artesunate,
pyronaridine, Fenozan B07,
trioxanes, nonane endoperoxides,
azithromycin, and WRZ38605.
PREVENTION AND
CONTROL
Personal protection
netting, screening,
protecting clothing and
repellents
Prophylactic treatment
Avoidance of sharing
IV needles
Thorough screening of
donor blood
PARASITE
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE NOTES
EPIDEMIOLOGY CLINICAL SYMPTOMS / TREATMENT
P.
malariae
See table below
Thin and thick blood films
w/ Giesma stains
Invade young RBCs
(as they are pliable)
Subtropic and
temperate
Quartan
malaria
Malarial
malaria
Take note
multiplies within
the confines of
mature RBCs.
Does not
contain
Ring stage not
commonly seen
Usually seen developing
trophozoite, immature and
mature schizonts
QUARTAN MALARIA
- incubation of 18-40 days followed by flu-like
symptoms
- cyclic paroxysms every 72 hrs
- no known relapses because dormant
hypnozoites are not associated with P. malariae
infections
TREATMENT
- quinine, quinidine, chloroquine, amodiaquine,
primaquine, pyrimethamine, sulfadoxine,
dapsone, mefloquine, tetracycline, doxycycline,
halofantrine, atovaquone, proguanil, ginghaosu,
artemisinin, artemether, artesunate,
pyronaridine, Fenozan B07, trioxanes, nonane
endoperoxides, azithromycin, and WRZ38605.
PREVENTION AND
CONTROL
Personal protection
netting, screening,
protecting clothing and
repellents
Prophylactic treatment
Avoidance of sharing IV
needles
Thorough screening of
donor blood
Control mosquito breeding
areas
PARASITE
MORPHOLOGY
LAB DIAGNOSIS
P.
falciparum
Thick blood films
screening
Black water
Thin blood films
speciation
fever
LIFE CYCLE
NOTES
Invade RBC at any
age
Infect up to 50% of
the RBC
population
Peripheral blood films
reveal ring forms
Schizogony
and gametocyte
occur in capillaries
and blood sinuses
Infect RBCs but do
not appear enlarged
Occur in the
or distorted
warmer months of
late summer and
Recrudescence may early autumn
occur and is fatal
Aka
aestivoautumnal
malaria
Malignant
tertian malaria
Aestivoautumnal
malaria
fnblertian
malaria
falciparum
malaria
Infects RBCs at any age
EPIDEMIOLOGY CLINICAL SYMPTOMS / TREATMENT
Tropical and
subtropical
regions
BLACK WATER FEVER AND
MALIGNANT TERTIAN MALARIA
- incubation of 7-10 days followed by
flu-like symptoms
- cyclic paroxysms every 36-48 hrs
- mimic those seen in malignant
tertian malaria
- most deadly form if malaria in
untreated patients
- Kidney involvement, known as
black water fever, usually results in
marked hemoglobinuria (the
presence of hemoglobin in the
urine) caused by P. falciparuminduced red cell destruction.
- Acute renal failure, tubular necrosis,
nephrotic syndrome and death
- Coma death
- Abdominal pain, vomiting of bile,
rapid dehydration and sever
diarrhea
TREATMENT
- quinine, quinidine, chloroquine,
amodiaquine, primaquine,
pyrimethamine, sulfadoxine,
dapsone, mefloquine, tetracycline,
doxycycline, halofantrine,
atovaquone, proguanil, ginghaosu,
artemisinin, artemether, artesunate,
pyronaridine, Fenozan B07,
trioxanes, nonane endoperoxides,
azithromycin, and WRZ38605.
- Malaria is treated first, then
secondary complicating health
problems
PREVENTION AND
CONTROL
Personal protection
netting, screening,
protecting clothing
and repellents
Prophylactic
treatment
Avoidance of
sharing IV needles
Thorough screening
of donor blood
Control mosquito
breeding areas
Vaccine
PARASITE
LAB DIAGNOSIS
LIFE CYCLE NOTES
CLINICAL SYMPTOMS / TREATMENT
PREVENTION AND CONTROL
P. knowlesi
DNA extraction and nested-PCR
examination of samples have been known
to reveal the differences between the two
Plasmodium species
resemble P.
falciparum
CLINICAL FEATURES
- Respiratory distress
Acute renal or multi-organ failure
- Shock
Personal protection netting,
screening, protecting clothing
and repellents
Giesma-stained peripheral blood films
specimen of choice
Wright stain (thick for screening; thin for
differentiate)
PCR
TREATMENT
- No complications
a. quinine,
b. chloroquine
c. artemetherlumefantrine
- severe
a. Inraveous quinine
b. artesunate
c. combination of chloroquine-primiquine
Prophylactic treatment
Avoidance of sharing IV needles
Thorough screening of donor
blood
Control mosquito breeding areas
Vaccine
CLASSIFICATION:
- Ciliates - parasites that move by means of hairlike
cytoplasmic extensions called cilia, contains one
human pathogen known as Balantidium coli
- Select Sporozoa – (excluding Plasmodium and
Babesis spp.) which are intestinal and tissue-dwelling in
nature, belong to the subclass Coccidia, a group of
protozoal parasites in which asexual replication occurs
outside a human host and sexual replication occurs
inside a humanhost, and are often referred to as
coccidian protozoans.
- Blastocystis hominis (Fig. 7-3), initially considered as a
yeast, makes up the third group and is now classified
as a Protozoa. This organism is the sole member of the
class Blastocystea.
- Pneumocystis jiroveci (formerly known as
Pneumocystis carinii) is the only member of the fourth
group (Fig. 7-4). This organism was traditionally
included with the Protozoa, even though it has been
recently reclassified as a fungus.
T. gondii (cont.)
- TOXOPLASMOSIS: GENERAL SYMPTOMS
a. Mild, mimic symptoms of infectious mononucleosis
b. Fatigue, lymphadenitis, chills, fever, headache and
myalgia
c. Maculopapular rash, encephalomyelitis,
myocarditis, hepatitis
d. Retinochoroiditis w/ subsequent blindness
- CONGENITAL TOXOPLASMOSIS
- Factors that affect its degree of severity:
1. Antibody protection from the mother
2. Age of the fetus at the time of infection
- Subsequent retinochoroiditis (years after initial
infection)
- CHILD: hydrocephaly, microencephaly,
intracerebral calcification, chorioretinitis,
convulsions, psychomotor disturbances
- Result: mental retardation, severe visual
impairment, or blindness
- TOXOPLASMOSIS IN IMMUNOCOMPROMISED
PATIENTS:
- Patients immunosuppressed because of organ
transplantation or the presence of neoplastic
disease, such as Hodgkin’s lymphoma, have long
been known to contract toxoplasmosis as an
opportunistic infection
- Screen potential donor units for toxoplasmosis prior
to transfusion
- CEREBRAL TOXOPLASMOSIS IN AIDS PATIENTS
- toxoplasmic encephalitis, CNS involvement
- early symptoms: headache, fever, altered mental
status (inc. confusion), lethargy
- developed to: subsequent focal neurologic deficits,
brain lesions, convulsions
- OTHER INFORMATION:
- do not spread into other organs of the body but
rather stay confined within the CNS
- diagnostic: rise in spinal fluid IgG antibody levels
(demonstration of tachyzoites in CSF)
- Most infected patients do not have serum levels of
IgM antibodies.
- The lack of serum IgM coupled with the lack of
change in serum IgG levels in these patients
suggests that their infections occurred because of a
reactivation of a chronic latent infection and not
because of an acquired primary infection.
PARASITE
MORPHOLOGY
Balantidium
coli
LAB DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY
CLINICAL SYMPTOMS /
TREATMENT
PREVENTION AND
CONTROL
stool specimens
initiated on
ingestion of
infective cysts in
contaminated food
or water.
Human infection is
very low
ASYMPTOMATIC: no symptoms
Personal hygiene
Balantidiasis:
- Mild colitis, diarrhea, fullblown clinical balantidiasis
- Mucosa and submucosa
abscesses and ulcers
- Secondary bacterial infection
- 15 liquid stools (w/ pus,
mucus, blood)
- CHRONIC: tender colon,
anemia, cachexia and
occasional diarrhea
- May invade liver, lungs,
pleura, mesenteric nodes and
urogenital tract
Proper sanitation
Sigmoidoscopy for
patients suffering
from sigmoid rectal
infection
Balantidiasis
wet preparations
and the permanent
stain
Trophozoite: aka Balantidium,
which means “little bag.”
excystation in the
small intestine
transverse binary
fission, from which
two young
trophozoites
emerge.
Encystation occurs
in lumen
Rare
transmitted by
ingesting
contaminated food
and water by the oralfecal and person-toperson routes.
TREATMENT:
- oxytetracycline (Terramycin)
and iodoquinol.
- Metronidazole (Flagyl)
Proper precautions
when handling and
dealing pigs and its
feces
PARASITE MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY
CLINICAL SYMPTOMS PREVENTION
/ TREATMENT
AND
CONTROL
Isospora
belli
Stool samples (immature,
partially or fully mature) –
Sheather’s sugar flotation
procedure
Coccidial parasite
Rare but has
worldwide geographic
distribution
ASYMPTOMATIC: no
symptoms
Isosporiasis
Duodenal contents
Enterotest (oocysts)
Intestinal biopsies
Oocysts – visible in direct
wet preparations, flotation
procedures or
concentration
- Transparent and can’t
be seen in saline wet
prep
- Seen better in iodin
wet prep
- zinc sulfate technique
or another
concentration
procedure following
polyvinyl alcohol
(PVA) preservation.
- Auraminerhodamine
permanent stain.
- Acid-fast stain
No intermediate host
Both asexual and
sexual reproduction
take place
Ingestion of ineffective
mature (sporulated)
oocytes
(gametogony) takes
place in the same
intestinal area.
Asexual reproduction
(schizogony)
Immature oocysts
typically complete their
development in the
outside environment.
mature sporulated
oocyst that is capable
of initiating another
infection.
Isosporiasis
An increase in
- mild gastrointestinal
reported cases began
discomfort to severe
to occur during and
dysentery.
following World War II. - weight loss, chronic
Specifically, cases
diarrhea, abdominal
were reported in
pain, anorexia,
Africa, Southeast
weakness, and
Asia, and Central
malaise
America.
- Charcot-Leyden
crystals,
Increase in patients
malabsorption
suffering from AIDS
syndrome
- foul-smelling stools
Oral anal sexual
that are pale yellow
contact mode of
and of a loose
transmission
consistency.
- Increased fecal fat
levels
- Infected patients
may shed oocysts in
their stools for as
long as 120 days.
Death may result
from such severe
infections.
TREATMENT:
- Bland diet and rest
- Chemotherapy (w/
trimethoprim and
sulfamethoxazole or
pyrimethamine and
sulfadiazine)
proper personal
hygiene
adequate
sanitation
practices
avoidance of
unprotected sex,
particularly
among
homosexual men.
PARASITE MORPHOLOGY
LAB
DIAGNOSIS
LIFE CYCLE NOTES
EPIDEMIOLOGY CLINICAL SYMPTOMS /
TREATMENT
PREVENTION AND
CONTROL
Sarcocystis
species
Stool
specimen
Routine
histologic
methods
In addition to its
presence in cattle
and pigs,
Sarcocystis spp.
may also be found
in a variety of wild
animals.
adequate cooking of
beef and pork
Sarcocystis
infection.
Asexual reproduction of
Sarcocystis occurs in the
intermediate host.
transmission occurs when
uncooked pig or cattle meat
infected with Sarcocystis
sarcocysts is ingested.
(Human is definitive host)
Transmission route occurs
when humans accidentally
swallow oocysts from stool
sources of animals other
than cattle or pigs(human is
the intermediate host)
*In many cases, only single or double
sporocysts cemented together may be visible
in stool samples.
Infections are
relatively low
SARCOCYSTIS
INFECTION:
- experienced fever, severe
diarrhea, weight loss, and
abdominal pain. It is
presumed that patients
suffering from muscle
tenderness and other local
symptoms
Treatment:
- Definitive host:
trimethoprim plus
sulfamethoxazole or
pyrimethamine plus
sulfadiazine
- Intermediate host: no
known chemotherapy
proper care and
disposal of animal
stool
PARASITE
Cryptosporidium
parvum
Cryptosporidosis
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY
CLINICAL
SYMPTOMS /
TREATMENT
PREVENTION
AND CONTROL
Stool specimen
Ingestion of mature
oocyst
Worldwide distribution
Cryptosporidiosis:
- Diarrhea: lasts 2
weeks, 1-4 weeks
in some daycare
centers.
- Fever, nausea,
vomiting, weight
loss, and
abdominal pain
may also be
present.
- Great fluid loss
may be fatal
- Malabsorption
Proper treatment of
water supplies, use
gloves, and wearing
gown
Iodine or modified
acid-fast stain.
Formalin fixed smears
stained with Giemsa
Enterotest,, enzymelinked immunosorbent
assay (ELISA)
excystation in the
upper
gastrointestinal tract,
Asexual and sexual
multiplication
Sporozoites rupture
Indirect
immunofluorescence
Thin cell:
autoinfection
Modified zinc sulfate
flotation or Sheather’s
sugar flotation
Thick cell: remains
intact and is passed
out of the body may
initiate autoinfection
occasionally
20 species known
only C. parvum infect
humans
Water or food
contamination
Person-to-person
AIDS patients risk of
contracting this
parasite
Children in tropical
areas, animal
handlers, travelers
abroad
TREATMENT:
- Spiramycin
(experimental)
Proper handwashing
and disinfecting
Enteric precautions
PARASITE
Blastocystis
hominis
Blastocystis
hominis
infection.
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE
NOTES
EPIDEMIOLOGY
CLINICAL
SYMPTOMS /
TREATMENT
PREVENTION AND
CONTROL
Stool specimen
sporulation or binary
fission.
Epidemics in
subtropical countries
participates in sexual
and asexual
reproduction, and
exhibits pseudopod
extension and
retraction.
From Saudi Arabia to
British Columbia.
BLASTOCYSTIS
HOMINIS INFECTION:
- diarrhea, vomiting,
nausea, and fever,
as well as
abdominal pain
and cramping.
Proper treatment of
fecal material,
thorough hand
washing
Iodine wet
preparations
Peripheral cytoplasm
appears yellow
central vacuole is
transparent
Permanent stain
preparations
Peripheral cytoplasm
dark stain central
vacuole not apparent
In water or saline
lyses may lead to
false-negative results
ingestion of fecally
contaminated food or
water.
TREATMENT:
- Iodoquinol or
metronidazole
subsequent proper
handling of food and
water
PARASITE
Cyclospora
cayetanensis
Cyclospora
cayetanensis
infection
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE NOTES
EPIDEMIOLOGY
CLINICAL SYMPTOMS /
TREATMENT
PREVENTION AND
CONTROL
stool samples
(concentrated
nontraditionally without
the use of formalin
fixative)
ingestion of an oocyst
many countries,
including the United
States and Canada
Cyclospora cayetanensis
Infection
- a longer duration of
diarrhea than
cryptosporidiosis.
- no known connection
between C.
cayetanensis infection
and
immunocompromised
patients
properly treating water
sporulate best at
room temperature
5% potassium
dichromate →
sporocysts become
visible
Flotation methods
Modified acid-fast stain
Oocysts auto fluoresce
under ultraviolet light
microscopy.
oocyst contains two
sporocysts, each
enclosing
two sporozoites
small intestine →
sporozoites → asexual
reproduction → macroand micro-gametocyte
production
Male and female
gametocytes unite and
form oocysts
Infected
humans pass immature
oocysts in the stool.
No animal reservoir
exists.
children living in
unsanitary
conditions in Lima,
Peru
travelers and
foreigners
residing in Nepal
and parts of Asia.
Contaminated
lettuce
and fresh fruit
using treated water
when handling and
processing food
PARASITE
Toxoplasma
gondii
Toxoplasmosis
congenital
toxoplasmosis
cerebral
toxoplasmosis
MORPHOLOGY
LAB
DIAGNOSIS
LIFE CYCLE NOTES
EPIDEMIOLOGY
CLINICAL
SYMPTOMS /
TREATMENT
PREVENTION AND
CONTROL
blood samples
using serologic
test
Definitive host: cat
found worldwide
enclosed bradyzoites:
transform into tachyzoites
(brain or muscle tissue)
populations at risk:
individuals suffering
from AIDS
avoidance of contact
with cat feces.
asexual and sexual
reproduction: gut of cat
occur in 15%
to 20% of the population
in the United States.
Asymptomatic:
- asymptomatic
- cause disease in
humans when:
1. a virulent strain of
the organism has
entered the body
2. the host is in a
particularly
susceptible state
(e.g., those
suffering from
AIDS)
3. the specific site
of the parasite in
the human body
is such that tissue
destruction is
likely to occur
recommended
test for the
determination of
IgM present in
congenital
infections:
doublesandwich
ELISA method
IgM and IgG –
IFA test
Other: IgG –
IHA and ELISA
sexual cycle results in the
production of immature
oocysts, shed in stool
complete maturation: outside
environment; 1-5 days
rodents – intermediate hosts
sporozoites → mature oocysts
→ tachyzoites (intestinal
epithelium) → migration →
brain or muscle → cysts w/
bradyzoites
human infection:
1. hand-to-mouth
transmission
2. human ingestion of
contaminated
undercooked meat from
cattle, pigs, or sheep
3. transplacental infection
4. contaminated blood is
transfused into an
uninfected person
consumption of
undercooked meat and
its juices by women and
their children in Paris
was reported in 93% (the
highest recorded rate)
and 50%
4000 infants born with
transplacentally acquired
T. gondii infections
wearing protective
gloves when cleaning
out
a cat litter box,
disinfecting the litter
box with
boiling water, and
thorough hand
washing afterward.
avoidance of ingesting
contaminated meat.
avoidance of tasting
raw meat
all meat should be
thoroughly cooked
keeping cats away
from potentially
infective rodents,
feeding cats only dry
or cooked canned
cat food, and/or not
having cats at all
PARASITE
Pneumocystis
jiroveci
Pneumocystosis
atypical
interstitial
plasma cell
pneumonia.
MORPHOLOGY
LAB DIAGNOSIS
LIFE CYCLE NOTES
EPIDEMIOLOGY
Histologic
procedures –
Gomori’s
methenamine silver
nitrate stain
presumed that
once inside the host, P.
jiroveci takes up
residence
in the alveolar spaces
in lung tissue.
Areas of particular
note include the
United States, Asia,
and Europe
Giemsa and iron
hematoxylin stains
may be used
serologic
techniques
monoclonal
immunofluorescent
sputum,
bronchoalveolar
lavage, tracheal
aspirate, bronchial
brushings,
and lung tissue
Mature cysts
rupture, producing
actively growing,
multiplying, and feeding
trophozoites. The
trophozoites
eventually convert into
precysts and cysts.
May invade spleen,
lung, lymph nodes and
bone marrow
CLINICAL SYMPTOMS /
TREATMENT
Pneumocystosis: Atypical
Interstitial Plasma Cell
Pneumonia:
- nonproductive cough,
fever, rapid respirations,
Organism
and cyanosis.
transmission: transfer - Interstitial plasma cell
of pulmonary droplets
pneumonia → cause of
through direct persondeath in AIDS patients
to-person contact
- Kaposi’s sarcoma
(AIDS patients)
People at risk:
- Infected malnourished
immunosuppressed
infants experience poor
patients (those w/
feeding, loss of energy,
AIDS), children and
a rapid respiration rate,
those with
and cyanosis.
predisposing
- infiltrate on chest x-ray
conditions
- Breathing difficulties
(PO2 (arterial oxygen
May pass through
tension) and a normal
placenta and cause
to low PCO2 (carbon
infection in the fetus
dioxide tension))
as well as stillbirth
- Prognosis is usually
poor
TREATMENT:
- Trimethoprimsulfamethoxazole
(Bactrim)
- Pentamidine isethionate
and cotrimoxazole
(alternative)
PREVENTION AND
CONTROL
personal protection
from these droplets
Protective gear, such
as a mask, worn
around known
infected persons
-
Roundworms are unembryonated, elongated,
cylindrical in shape.
With sensory organs known as chemoreceptors
The sexes are separate
Female may be
a. oviparous producing eggs that hatch outside the body
b. viviparous giving birth to tiring young
c. larviparous larvae bearing i denoting passage of larvae rather
than uggs
3 basic morphologic forms:
1. eggs (female sex cells after fertilization) very in
size and shape
2. larvae (juvenile worms) typically long and slender
3. adult worms females are longer than males,
complete digestive and reproductive system
digestive system:
1. mouth hooks, teeth, plates, and other structures
2. buccal cavity tubular or funnel-shaped
3. esophagus a muscular tube that pumps food
posteriorly into the intestine
4. intestine a flattened tube with a wide lumen that
follows a straight course from the esophagus to the
rectum
5. rectum defecation occurs when the anus is
dilated and the pseudocoel pressure forces the
feces out
-
-
-
-
-
-
NEMATODE CLASSIFICATION
Based on the presence or absence of caudal
chemoreceptor organ
Class Enoplea (class
Class Rhabditea (Class
Adenophorea; class
Secernentia; Class
Aphasmidea)
Phasmidea)
- Without caudal
with caudal
chemoreceptor organ
chemoreceptor organ
(phasmids):
(phasmids)
1. Trichuris trichiura
1. Ascaris lumbricoides
2. Trichinella spiralis
2. Strongyloides
3. Capillaria philippinensis
stercoralis
3. Enterobius
vermicularis
4. Angiostrongylus
cantonensis
5. Filarial worms
6. Hookworms
7. Dracunculus
medinensis
Classification according to habitat:
Intestinal nematodes
Extraintestinal nematodes
1. Enterobius
1. Trichinella spiralis
vermicularis
2. Dracunculus
2. Trichuris trichura
medinensis
3. Ascaris
3. Filarial worms
lumbricoides
4. Necator
americanus
5. Ancylostoma
duodenale
6. Strongyloides
stercoralis
7. Capillaria
philippinensis
LIFE CYCLE NOTES
1. Direct (homogonic)
- Require DH but not IH
- Homoxenous
2. Indirect (heterogonic)
- Require both DH and one or more IH
- Heteroxenous
LABORATORY DIAGNOSIS
- Recovery of eggs, larvae, and occasional adult worms
- Cellophane tape prep (around the anal opening)
- Stool samples
- Tissue biopsies
- Infected skin ulcers
- Serologic tests
PATHOGENESIS AND CLINICAL SYMPTOMS
- FACTORS:
1. Number of worms present
2. Length of time the infection persists
3. Overall health of the host
- Infections with nematodes may last up to 12 months or
longer
- Occurrence of reinfections may increase the infection
time up to several years and beyond
- (with an exception) all the nematodes may cause
intestinal infection symptoms at some point during their
invasion of the host
a. Abdominal pain
b. Diarrhea
c. Nausea
d. Vomiting
e. Fever
f. Eosinophilia
g. Skin irritation
h. Skin blister
i. Muscle involvement
Enterobius vermicularis
Trichuris trichiura
Trichuris trichiura egg
Ascaris lumbricoides
Ascaris lumbricoides, decorticated unfertilized egg
Ascaris lumbricoides, adult female.
Necator americanus
Hookworm egg
Strongyloides stercoralis
Trichinella spiralis
Trichinella spiralis larvae in muscle press.
Parasite
Enterobius
vermicularis
Pinworm
seat worm
Morphology
Laboratory
diagnosis
Cellophane tape
prep collected from
the perianal region
Multiple samples
may be required to
confirm the presence
of a light infection
and to detect free
from infection
May be recovered
from stool samples
Life cycle notes
Epidemiology
Humas only known
host
Temperate areas
Self-limiting initiated
following the ingestion
of the infective eggs
Digestive tract small
intestine (hatch &
release young larvae)
grow and mature
adult worms (in colon)
15k eggs deposit
(perianal region)
Most common
helminth known to
cause infection in
the US
Hand-to-mouth
contamination
Most
contract
4-6 hrs incubation
developing eggs
achieve infective status
RETROINFECTION
infective pinworm eggs
that migrate back into
the host body
AUTOREINFECTION
infected individuals
reinfect themselves
bpnlation mating of
-
Gravid
-
worms
pregnant female
worm
to
child
-
Morphologic forms
in
select
likely
recovered
cases
↳ eggs
&
adult
females
Clinical
Prevention and
ETEROBIASIS:
pinworm infection
- Intense itching
- Pruritus ani
- Inflammation of the
anal and/or vaginal
areas
- Intestinal irritation
- Mild nausea
- Vomiting
- Irritability
- Difficulty sleeping
- Minute ulcers
- Mild intestinal
inflammation
- Abdominal pain
Proper hand washing
symptoms/treatment
ASYMPTOMATIC no
clinical symptoms
TREATMENT
- Albendazole
- Mebendazole
- Pyrantel pamoate
control
Practice proper
personal hygiene
Applying an ointment
or salve to an infected
perianal area to
prevent egg dispersal
into the environment
Avoid scratching the
infected area
Thorough cleaning of
environmental
surfaces
Total eradication is
highly unlikely
(
Parasite
Morphology
Trichuris
trichiura
Whipworm
Laboratory
diagnosis
Stool (eggs)
processed using
zinc sulfate
flotation method
Life cycle notes
Epidemiology
Ingestion initiates human
infection
Found in warm
climates w/ poor
sanitation
practices
Eggs larvae (small intestine)
growth and development
otw to intestinal lumen
cecum (complete maturation)
Macroscopic
examination of
intestinal
mucosa, rectum Resulting adults take up
and intestinal
residence in the colon,
tract ( adult worms) embedding in the mucosa
4-8 years lifespan of adult
sulfate flotation worms in untreated infections
method
zinc
Eggs
-
characterized
by presence of
hyaline polar plugs
Adult male
- usually smaller than the adult female.
- Contains easily recognizable curled tail
3rd most
common
helminth
Areas in US inc.
warm humid
south (rural
settings)
At risk: children
and those in
psychiatric
facilities
Clinical
Prevention and
TRICHURIASIS:
whipworm infection:
- Heavy infections:
500-5000 worms
- In children:
ulcerative colitis
- 200 worms in
children:
1. Chronic
dysentery
2. Severe anemia
3. Growth
retardation
4. Catch up growth
occurs
5. Rectal prolapse
6. Peristalsis
- In adults:
1. inflammatory
bowel disease.
2. Abdominal
tenderness and
pain
3. Weight loss
4. Weakness
5. Mucoid or
bloody diarrhea
Avoidance of
defecating directly
into the soil
symptoms/treatment
ASYMPTOMATIC no
clinical symptoms
TREATMENT
- Albendazole
- Mebendazole
control
Practice proper
personal hygiene
Avoid usage of
feces as fertilizer
Avoid placing
potentially infective
hands into the
mouth
Thorough
treatment of
infected people
Parasite
Morphology
Ascaris
lumbricoides
roundworm
man
Life cycle notes
Epidemiology
Stool (eggs)
Ingestion of infected
eggs that contain
viable larvae
Most common
helminth infection
in the world
In small intestine
larvae emerge from
the eggs migrate
from liver to lungs by
entering blood via
penetration through
the intestinal wall
Found in warm
climates and
areas of poor
sanitation
ADULT WORMS may be
recovered in small intestine,
gallbladder, liver, appendix,
stool, vomit, external nares
large intestinal
Roundworm
Laboratory diagnosis
of
Liver lung
capillaries alveoli
bronchioles
pharynx (by cough)
swallowed
intestine
250k eggs passed in
the feces
Eggs may survive in
10% formalin fixative
used in stool
processing
Layers of egg:
a. Inner - Vitelline membrane
b. Middle - Glycogen layer
c. Outermost - Albuminous/mammilary
coat
Decorticated term that describes the lack of
-
an
outer
coating
mammalian
albuminous
At risk: children
who place their
contaminated
hands into their
mouths, those
who ingest
vegetables that
were grown using
contaminated
human feces as
fertilizer
Clinical
Prevention and
ASCARIASIS: roundworm
infection
- Single worm:
1. Tissue damage
2. Secondary bacterial
infection
- Many worms:
1. Vague abdominal
pain
2. Vomiting
3. Fever
4. Distention
5. Obstruction of
intestine, appendix,
liver, bile duct
6. Discomfort in areas
where the worms
may exit (anus,
mouth or nose)
7. Protein malnutrition
8. Pulmonary symptoms
9. Low-grade fever
10. Cough
11. Eosinophilia
12. Pneumonia
13. Asthmatic reactions
Proper sanitation
symptoms/treatment
ASYMPTOMATIC no
clinical symptoms
TREATMENT
- Albendazole
- Mebendazole
- Other that are
designed to get rid
the body of the
parasitic worms
control
Practice proper
personal hygiene
Avoidance of using
human feces as
fertilizer
Parasite
Morphology
Necator
americanus
Laboratory
diagnosis
Stool (eggs)
Larvae may matura
Man
and hatch from the
eggs in stool that
has been allowed to
sit at room temp
(without fixative
added)
New World
hookworm
Buccal capsule is
necessary to
determine the
specific hookworm
organism
Anglo stoma
-
adult
hookworm that
is
characterized by a
buccal cavity that
contains tooth
skin
-
Buccal capsule is provided with semilunar cutting
plates
Equipped with an amphidial gland
Tail contains a copulatory bursa and copulatory
spicule
common name: old world hookworm
Diseases: Ancylostomiasis and
anemia
Characteristic shape of adult is letter C
Adult worm has 2 pairs of ventral teeth
Has a pair of copulatory spicule which is bristle like
penetration
Life cycle notes
Epidemiology
3rd-stage filiform
larvae penetrate
through the skin
e.g. unprotected
feet
population is
infected with
hookworms
Migrate to
lymphatics and
blood system
Blood carries the
larvae to the lungs
penetrate the
capillaries enters
alveoli migrate
to bronchioles
coughed up
(pharynx)
swallowed
deposited into the
intestine
Maturation occurs in
the intestine
Adult females lay
10k 20k eggs/day
Found in warm
areas
Areas w/ poor
sanitation
practices
May be found in
SA, Europe,
china, Africa, SA,
Caribbean
Clinical
Prevention and
TREATMENT: adequate diet
rich in iron, protein and other
vitamins
Proper
sanitation
symptoms/treatment
ASYMPTOMATIC no clinical
symptoms.
HOOKWORM DISEASE:
ancylostomiasis, necatoriasis
- Itching at the site (ground
itch)
- Sore throat
- Blood sputum
- Wheezing
- Headache
- Mild pneumonia with
cough
<500 eggs
- Vague mild GI symptoms,
slight anemia, weight loss,
weakness
>5000 eggs
- Diarrhea, anorexia,
edema, pain, enteritis and
epigastric discomfort
- Microcytic hypochromic
iron deficiency, weakness
and hypoproteinemia and
mortality
TREATMENT
- Pyrantel pamoate
- Mebendazole
- Iron replacement and
other dietary therapy
control
Practice proper
personal
hygiene
Prompt and
thorough
treatment of
infected people
Personal
protection of
people e.g.
covering bare
feet
Parasite
Morphology
Laboratory
Life cycle notes
Epidemiology
Clinical symptoms/treatment
diagnosis
Strongyloides
sterocoralis
Stool (diagnostic
eggs)
concentrated with
zinc sulfate
Threadworm
Diagnostic
rhabditiform larvae
may be recovered
in fresh stool
samples and
duodenal aspirates
Enterotest
Sputum samples
control
3 routes
Tropical and
subtropical
regions
:
1) Direct
a) Indirect
3) Anto infection
Areas of the
South
Appalachian
Mountain region
DIRECT
Rhabditi form larvae
-
in the
passed
feces
develop directly into
↳
3rd stage infective
the
Hari form
warm
larvae in
moist soil
,
.
Serologic tests (inc.
ELISA)
INDIRECT
rhabditiform
thread worm
larvae
passed
-
into the
outside environment &
mature into
(
adults
↳
non
produce
-
free-living
parasitic)
eggs that
develop into
rhabditform
larvae
↳ mature
→
filaform
stage
Common name: Threadworm
- Adult contains short buccal cavity and a long
esophagus
- Body of the worm is transparent with fine striated
cuticle
- Ova has a characteristic Chinese lantern shape
- Diseases: Strongyloidiasis and Cochin china
diarrhea
Prevention and
AUTO INFECTION
Rhabditi form
larvae
initiates
new
of
→
infective
larvae
t
enters the
a
cycle
infection
c-
lymphatic
system
Areas of poor
sanitation
At risk: those who
come into skin
contact with
contaminated soil
and those in poor
sanitation
practices (e.g.
psychiatric
facilities)
ASYMPTOMATIC no clinical
symptoms.
STRONGYLOIDIASIS:
threadworm infection
- Diarrhea
- Abdominal pain
- Urticaria w/ eosinophilia
- Vomiting
- Constipation
- Weight loss
- Variable anemia
- Malabsorption syndrome
- Site of larvae penetration
becomes itchy and red
- Pulmonary symptoms
- Recurring allergic
reactions
- Immunocompromised
people may suffer from
severe autoinfections
(leads to spread of larvae
throughout the body,
increase secondary
bacterial infections and
death)
TREATMENT
- Ivermectin
- Albendazole
Practice proper
personal
hygiene
Proper
sanitation
Proper handling
and disposal of
fecal material
Adequate
protection of the
skin
Treatment of
infected people
Parasite
Morphology
Laboratory diagnosis
Life cycle notes
Epidemiology
Clinical symptoms /treatment
Prevention and
control
Trichinella
spiralis
Trichina
Worm
Affected skeletal muscle accidental human
infection with a
Serologic methods
parasite whose
normal host is an
Other indicators:
animal (zoonosis)
leukocytosis and
eosinophilia, elevated
consumption of
serum muscle enzyme
undercooked
levels
contaminated meat
(striated muscle)
No known test is
Ingested larvae
completely 100%
t
accurate
intestine (maturation)
t
mating
to
gravid
to
female migrates
adult
intestinal snbmnwsa
t
lays
larvae
her
tire
t.no
)
egg stage
t
infant
blood
enters
t
travel
striated muscle
to
to
unapt
cells
nurse
to
granuloma forms
to
calcification
completion of
doesn't
life
cycle
larvae
T
.
spiralis
occur
ceases
encysts
when
Found worldwide
except the tropics
(Members of the
meat-eating
populations)
TRICHINOSIS,
TRICHINELLOSIS
Light infection:
1. Diarrhea
2. Slight fever
- Heavily infected:
May be found in pig,
1. Vomiting
deer, bear, walrus
2. Nausea
and rate
3. Abdominal pain.
Diarrhea
Resistant to colder
4. Headache
regions
5. Fever
- When larvae begin their
Feeding of
migration:
contaminated pork
1. Eosinophilia
scraps to hogs
2. Pleural area pain
accounts for a
3. Fever
major mode of its
4. Blurred vision
transmission
5. Edema
6. Cough
7. Death
- When larvae is settled in
the striated muscle and
encystation begins:
1. Muscular discomfort
2. Edema
3. Local inflammation
4. Overall fatigue
5. weakness
TREATMENT:
- non-life threatening: no
meds (get rest, fluids, fever
reducers, pain relievers)
- life threatening:
prednisone, thiabendazole
Thorough cooking of
meats
Proper storage of
meats
15° C
[59° F] for 20 days or
days
Avoidance of feeding
pork scraps to hogs
Parasite
Morphology
Laboratory diagnosis
Life cycle notes
Epidemiology
Clinical symptoms
Prevention and
control
Dracunulus
medinensis
Observing infected
ulcers
Guinea
Induced rupture of the
infected ulcers by
immersing in cool
water reveals the firststage larvae
worm
Ingestion of drinking
water contaminated
with infected copepods
(freshwater fleas)
infected ulcer
results at the site of
the larvae deposit.
ulcer ruptures and
releases the larvae
into the water.
Copepods living in the
water consume the
first-stage larvae,
serving as its
intermediate host.
larvae
of
Ingestion
t
intestine
-
larvae
adult
→
worms
to
intestinal
penetrate
Fresh water
(step wells)
Ponds, human
made water
holes and
standing water
Reservoir hosts:
inc. dogs
GUINEA WORM
INFECTION:
Dracunculosis,
Dracunculiasis
- allergic reactions
- secondary bacterial
infection
- disabilities
- mortality
- painful ulcer (Once the
gravid female settles
into the subcutaneous
tissues and lays her
larvae)
- subsequent toxic
reactions in the ulcer
- nodule formation
- death and calcification
of an adult worm
TREATMENT
- total worm removal
use of properly
treated water for
consumption
boiling water
suspected of
contamination
prohibiting the
practice of drinking
and bathing in the
same water
ceasing the
practice of allowing
standing water to be
ingested
use a filter (finely
meshed filter)
educate the people
wall
to
connective tissues
or
body
cavities
&
gravid female migrate
to
skin
to
lay
live
first stage
-
larvae
to
adult
the
female may
body
deposit
into
site
at
/
deeper
(becomes
escape from
the larvae
migrate back
tissues
absorbed
)
check steps
highly unlikely of
total eradication
Ancylostoma braziliense
- Common name: Cat hookworm
- Disease: Cutaneous larva migrans / creeping eruption
- Adults have a pair of teeth and a pair of inconspicuous median teeth
- Copulatory bursa is broad and long with short lateral rays
Ancylostoma caninum
- Common name: Dog hookworm
- Disease caused: Cutaneous larva migrans/creeping eruption and eosinophilic
enteritis
- Adult worm has 3 pairs of ventral teeth
- Cephalic amphidial gland
HISTOLOGY SARCODINA HANDOUT
SUBPHYLUM SARCODINA
Subphylum
Sarcodina
Class
Lobosea
Intestinal Species
Entamoeba histolytica
Entamoeba hartmanni
Entamoeba coli
Entamoeba polecki
Endolimax nana
Iodamoeba b𝑢̈ tschlii
Extraintestinal Species
Entamoeba gingivalis
Naeglaria fowleri
Acanthamoeba species
•
•
GENERAL RULES
•
•
•
•
•
SUBPHYLUM: SARCODINA
• Organism is generally known as AMEBAE
•
•
•
•
•
•
•
Entamoeba histolytica – pathogenic
(disease causing)
Entamoeba dispar – (morphologically
the same with histolytica) but different
rna and dna
Entamoeba moshkovskii – classified as a
free-living microorganism.
(Morphologically the same with
histolytica)
o Laredo stain
Entamoeba hartmanni - (morphologically
the same with histolytica) but can be
differentiated through size.
o Small race E. histolytica
Entamoeba Coli
Endolimax nana – smallest amoeba
o Comparable to the size of your
red blood cells
Entamoeba gingivalis – found most likely
in the oral cavity
Iodamoeba butschii – has a high affinity
to iodine
Entamoeba polecki – found most likely in
pigs and monkeys.
•
•
Commensals – except E. histolytica
(pathogenic)
Encystation – except E. gingivalis (does
not have a cystic stage)
Infected Stage: Cyst – except E. gingivalis
(does not have a cystic stage)
Mode of transmission: ingestion (except
for gingivalis: through mouth-to-mouth
contact)
Habitat: Large intestine (except for
gingivalis: oral cavity)
Locomotor organelle: Pseudopodium –
cell membrane extension
Multiplies through: Binary Fission
PSEUDOPOD
MORPHOLOGIC FORMS:
CYST:
•
•
Dominant stage
Non-motile
•
Formed stools
TROPHOZOITE
•
•
Feeding stage
Vegetative stage
BASIC STRUCTURE OF AMEBAE:
•
•
•
•
•
PSEUDOPODS: Often referred to as false
feet
KARYOSOME: Also referred to as
karyosomal chromatin; small central
mass of chromatin
PERIPHERAL CHROMATIN: A chromatin
material that surrounds the karyosome
CHROMATOIDAL BARS: Structures that
contain condensed RNA material
GLYCOGEN MASS: Cytoplasmic area
without defined borders that is believed
to represent stored food
CLASSIFICATION OF INTESTINAL
PROTOZOA
TRUE AMOEBA
•
SIGNIFICANCE
TWO REASONS:
1. Mistaken for the pathogenic entamoeba
histolytica
2. Indication of fecal contamination of food
and water
ENDOLIMAX NANA
•
•
•
•
Entamoeba
o Peripheral Chromatin
o Chromatoidal bodies
OTHER AMOEBA
•
COMMENSAL AMEBAE
Endolimax and Iodamoeba
o No peripheral chromatin
o Chromatoidal bodies are absent
DIFFERATIATING AMEBAE
•
Commensal
Smallest amoeba
Cross-eyed cyst
Cyst
o 5 -12 um
o Spherical, Ovoid, and Ellipsoid
o One – four nuclei
o Large and Blot-Like
o Cross-eyed cyst
Trophozoite
o 5 – 12 um
o Irregular
o Mononucleated
o Large and Blot-Like
o Granular and vacuolated
o Blunt Pseudopods
o Sluggish
IODAMOEBA BUTSCHLü
•
•
•
Commensal
Iodine Cyst
Large glycogen vacuole
•
Cyst
o 9 – 10um (6-16)
o Spherical to Ellipsoidal
o Mononucleated
Trophozoite
o 9-14um (4-20)
o Irregular
o Mononucleated
o Bacteria, yeast cells, and other
debris
•
ENTAMOEBA HISTOLYTICA
AMOEBIASIS
•
•
•
•
•
•
•
Pathogenic
Amoebic Dysentery
Colitis and Liver abscess
Flask-shaped ulceration
Gal/ Gal Nac lectin
Cysteine proteinases
Amebapores
VIRULENCE FACTORS
•
•
•
•
Adhesion molecules (N-acetyl-Dgalactosamine inhibitable lectine
Gal/GalNac – adhesion to colonic mucine
and host cells
o Induce contact dependent
cytolysis
Channel-forming peptides
(Amoebapores): Stored in cytoplasmic
granules and release following target cell
contact, forms iron exchanging channels
in plasma membrane – lysing the target
cells
Cystein protinases – Aid in penetration
of host tissue by digesting extracellular
matrix, cleaving collagen, elastin,
fibrinogen in extracellular matrix by
stimulating host cell proteolytic cascade
Resistance to host response
o Complement resistanceinactivates the complement
factors and are thus resistant to
complement mediated lysis.
o Limit the effectiveness of
humoral response by degrading
both IgA and IgG
ENTAMOEBA HISTOLYTICA
•
•
•
•
Cyst
o 10-20um
o Spherical to round
o One- four nuclei
o Small and central karyosome
o Bull’s eye cyst
Fine and evenly distributed
Peripheral chromatin
Rod. Cigar, sausage, and coffin shaped
ASYMPTOMATIC CARRIER STATE
•
•
•
•
•
Trophozoite
o 12-60um
o Irregular
o Mononucleated
o Small and central karyosome
o Fine and evenly distributed
o Peripheral chromatin
Hematophagous trophozoite
Clean-looking
Dendritic or Fingerlike
Directional and progressive
Entamoeba histolytica
THREE FACTOS:
1. Low virulence strain
2. Inoculation into the host is slow
3. Patient’s immune system is intact
PHOTOGENESIS AND CLINICAL
MANIFESTATIONS:
•
•
•
•
Amebic colitis
Amebic liver abscess
Ameboma
Flask-shaped ulcer
FLASK-SHAPED ULCERATION
Bacillary Dysentery
May be epidemic
Acute onset
Prodromal fever
and malaise
common
Vomiting common
Patient prostrate
Watery, bloody
diarrhea
Odorless stool
Stool microscopy:
numerous bacilli,
pus cells
Macrophages. Red
cells, no charcotleyden crystals
Abdominal cramps
common and
severe
Tenesmus common
Natural history:
Spontaneous
recovery in a few
days, weeks or
more; no relapse
Amebic Dysentery
Seldon epidemic
Gradual onset
No prodromal
features
No vomiting
Patient usually
ambulant
Bloody diarrhea
Fishy odor stool
-
FECAL OCCULT BLOOD TEST
•
Stool microscopy:
few bacilli, red cells,
trophozoites with
ingested red blood
cells, charcotleyden crystals
Mild abdominal
cramps
Tenesmus
uncommon
Natura; history:
lasts for weeks;
dysentery returns
after remission;
infection persists
for year
Occult blood – “Hidden blood”
o A. Used for early detection of
colorectal cancer
o B. Principle – pseudoperoxidase
activity of hemoglobin releases
oxygen from hydrogen peroxide
to oxidize guaiac reagent
o Interpretation – blue color
indicates gastrointestinal
bleeding
LABORATORY DIAGNOSIS:
•
•
•
•
•
Direct Fecal smear:
o Saline solution: trophozoite
motility
o Saline sol’n + MB: Entamoeba
spp. Will stain blue
o Saline sol’n + iodine: nucleus and
karyosome can be observed
Concentration techniques: FECT & MIFC
Culture: Robinson’s and Inoki medium
Serologic Testing: ELISA, IHAT, CIE, AGD
& IFAT
PCR, Ct-scan and MRI
CULTURE MEDIA
•
Witch of whished broomstick
•
Trophozoite
o 15-50um
o Irregular shape
o Mononucleated
o Eccentric karyosome
o Irregular peripheral chromatin
Dirty-looking
o Broader and blunter
pseudopodia
o Sluggish, non-directional, nonprogressive
ENTAMOEBA HISTOLYTICA
•
•
•
•
•
•
Robinson’s medium
Jones medium
Rice egg saline medium
Boeck and drbohlav medium
Diamond culture medium
Balamuth egg yolk infusion
Treatment
•
•
Metronidazole
Diloxanide furoate
Candidate Vaccine Molecules:
•
•
•
SREHP
Gal/GalNac lectin
Cysteine-rich amoebic antigen
ENTAMOEBA COLI
•
•
Commensal
Harmless inhabitant of the colon
•
Cyst
o 10-35 um
o Rounded or elongated
o 5-8 nuclei with eccentric
karyosome
o Irregular peripheral chromatin
Splinter needles
•
•
TROPHOZOITE
Movement
Shape of
pseudopodia
ENTAMOEBA
HISTOLYTICA
Unidirectional
ENTAMOEBA
COLI
Blunted
Manner or
release of
pseudopodia
Nucleus
Cytoplasm
Inclusion
Size
CYST
No. of nuclei
Chromatoidal
bar
Nuclear
membrane
Explosive
Uninucleated
Dirty looking
RBC
Smaller
ENTAMOEBA
HISTOLYTICA
Quadrinucleated
ENTAMOEBA
COLI
Broomstick,
splinter-like
Thin
ENTAMOEBA DISPAR
• Entamoeba histolytica
• Different DNA and Ribosomal RNA
• Isoenzyme pattern
ENTAMOEBA MOSHKOVSKII
• Entamoeba histolytica; Entamoeba
dispar
• Biochemically and genetically
• First detected in sewage
• Osmotolerant
• Ribodeme 2
ENTAMOEBA HARTMANNI
• Entamoeba histolytica
• Small race
• Cyst
o 4-10um
o Quadrinucleated
o Rod-shaped chromatoid
material with rounded or
square ends
• Trophozoite
o 3-10um
o Does not ingest red blood
cells
ENTAMOEBA POLECKI
• Rarely it can infect humans
• Pigs and monkeys
• Cyst
o Consistently uninucleated
o Angular or pointed
chromatoidal bars
• Trophozoite
o Small karyosome centrally
located
o Sluggish
ENTAMOEBA GINGIVALIS
• Found in the mouth
• : Kissing, droplet spray, or by
sharing of the utensils
• Does not undergoes encystation
• Trophozoite
o Surface of gum, teeth, in
gum pockets, and
sometimes in tonsillar crypts
• 10-20um
• Blunt pseudopods
• Bacteria
o Numerous
• Food vacuoles
o Mostly leukocytes
ENTAMOEBA CHATTONI
• Apes and monkeys
• Identical entamoeba polecki
• Isoenzyme analysis
FREE-LIVING PATHOGENIC AMEBAE
NAEGOLERIA FOWLERI
• Free-living amebae
• Primary amoebic meningoencephalitis
• Virulence factors:
o Phospholipase
o Sphingomyelinase
• Life cycle stages:
o Trophozoite
▪ Ameba
o Swimming form
▪ Flagellate
o Cyst
ACANTHAMEOBA SPP.
• Free-living amebae
• Acanthamoeba keratitis
• Granulomatous amebic
encephalitis
• Cutaneous acanthamebiasis
• Trophozoite stage
o Acanthopodia
o Thorn-like appendages
• Life Cycle stages
o Trophozoite
o Cyst stage (wrinkled cyst)